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1

Rao, Reena, Ming-Zhi Zhang, Min Zhao, et al. "Lithium treatment inhibits renal GSK-3 activity and promotes cyclooxygenase 2-dependent polyuria." American Journal of Physiology-Renal Physiology 288, no. 4 (2005): F642—F649. http://dx.doi.org/10.1152/ajprenal.00287.2004.

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The use of LiCl in clinical psychiatry is routinely complicated by overt nephrogenic diabetes insipidus (NDI), the mechanism of which is incompletely understood. In vitro studies indicate that lithium can induce renal medullary interstitial cell cyclooxygenase 2 (COX2) protein expression via inhibition of glycogen synthase kinase-3β (GSK-3β). Both COX1 and COX2 are expressed in the kidney. Renal prostaglandins have been suggested to play an important role in lithium-induced polyuria. The present studies examined whether induction of the COX2 isoform contributes to LiCl-induced polyuria. Four d
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2

Hao, Chuan-Ming, Martin Kömhoff, Youfei Guan, Reyadh Redha, and Matthew D. Breyer. "Selective targeting of cyclooxygenase-2 reveals its role in renal medullary interstitial cell survival." American Journal of Physiology-Renal Physiology 277, no. 3 (1999): F352—F359. http://dx.doi.org/10.1152/ajprenal.1999.277.3.f352.

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Renal medullary interstitial cells (MICs) are a major site of cyclooxygenase (COX)-mediated PG synthesis. These studies examined the role of COX in MIC survival. Immunoblot and nuclease protection demonstrate that cultured MICs constitutively express COX2, with little constitutive COX1 expression. SC-58236, a COX2-selective inhibitor, but not SC-58560, a COX1 inhibitor, preferentially blocks PGE2 synthesis in MICs. Transduction with a COX2 antisense adenovirus reduced MIC COX2 protein expression and also decreased PGE2production. Antisense downregulation of COX2 was associated with MIC death,
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3

Ricketts, Anthony P., Kristin M. Lundy, and Scott B. Seibel. "Evaluation of selective inhibition of canine cyclooxygenase 1 and 2 by carprofen and other nonsteroidal anti-inflammatory drugs." American Journal of Veterinary Research 59, no. 11 (1998): 1441. http://dx.doi.org/10.2460/ajvr.1998.59.11.1441.

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Abstract Objective To evaluate the activity of carprofen and other nonsteroidal anti-inflammatory drugs (NSAID) against isozymes of canine cyclooxygenases (COX1 and COX2). Procedure Constitutive COX1 was obtained from washed canine platelets, and COX2 was obtained from a canine macrophage-like cell line that was induced with endotoxin. Activity of carprofen and other NSAID against COX1 and COX2 was compared. Dose-response curves were plotted, and calculations were performed to identify concentrations that caused 50% inhibition (IC50[μM]) for each isozyme. Ratio of the COX1-to-COX2 IC50 was use
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4

Chen, Haolin, Lindi Luo, June Liu, and Barry R. Zirkin. "Cyclooxygenases in Rat Leydig Cells: Effects of Luteinizing Hormone and Aging." Endocrinology 148, no. 2 (2007): 735–42. http://dx.doi.org/10.1210/en.2006-0925.

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Previous studies suggested that increased Leydig cell cyclooxygenase (COX)2 expression may be involved in the reduced testosterone production that characterizes aged Leydig cells. Our objective herein was to further elucidate the relationships among LH stimulation, Leydig cell COX2 and COX1 expression, aging, and testosterone production. Incubation of Leydig cells from young or aged rats with LH or dibutyryl cAMP resulted in increases in both intracellular COX2 protein expression and testosterone production. COX1 expression did not respond to LH or dibutyryl cAMP. Incubation of adult cells wit
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5

Ren, Rongqin, Peter C. Charles, Chunlian Zhang, Yaxu Wu, Hong Wang, and Cam Patterson. "Gene expression profiles identify a role for cyclooxygenase 2–dependent prostanoid generation in BMP6-induced angiogenic responses." Blood 109, no. 7 (2006): 2847–53. http://dx.doi.org/10.1182/blood-2006-08-039743.

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Abstract The bone morphogenetic protein (BMP) family of proteins participates in regulation of angiogenesis in physiologic and pathologic conditions. To investigate the molecular mechanisms that contribute to BMP-dependent angiogenic signaling, we performed gene expression profiling of BMP6-treated mouse endothelial cells. We detected 77 mRNAs that were differentially regulated after BMP6 stimulation. Of these, cyclooxygenase 2 (Cox2) was among the most highly up-regulated by BMP stimulation, suggesting a role for Cox2 as a downstream regulator of BMP-induced angiogenesis. Up-regulation of Cox
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6

Mohammed Al bratty, Mohammed Al bratty, Neelaveni Thangavel Neelaveni Thangavel, Hassan Ahmad Alhazmi Hassan Ahmad Alhazmi, et al. "Gas Chromatography-Mass Spectrometry-based Phytochemical Analysis and In-Vitro Anti-Lipid Peroxidation, Cyclooxygenase Inhibition Activities of Saudi Eruca sativa Leaves." Journal of the chemical society of pakistan 44, no. 2 (2022): 175. http://dx.doi.org/10.52568/001001/jcsp/44.02.2022.

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Eruca sativa is a wholesome yearly shrubbery herb in Saudi Arabia. Eruca sativa leaves are a conventional food and are consumed raw in salads. The present research reports the phytochemical analysis, in-vitro anti-lipid peroxidation, total anti-oxidant capability, cyclooxygenase-1, and -2 (COX1 and COX2) inhibition activities of Saudi Eruca sativa leaves water decoction (EWD). Gas chromatography-mass spectrometry (GC-MS) of EWD revealed seventeen constituents of six different chemical groups: phenolics (23.60%), aromatic and aliphatic esters (16.97%), terpenoids (31.91%), heterocyclics (14.83%
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7

Upmacis, Rita K., Wendy L. Becker, Donna M. Rattendi, et al. "Analysis of Sex-Specific Prostanoid Production Using a Mouse Model of Selective Cyclooxygenase-2 Inhibition." Biomarker Insights 17 (January 2022): 117727192211421. http://dx.doi.org/10.1177/11772719221142151.

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Background: Prostanoids are a family of lipid mediators formed from arachidonic acid by cyclooxygenase enzymes and serve as biomarkers of vascular function. Prostanoid production may be different in males and females indicating that different therapeutic approaches may be required during disease. Objectives: We examined sex-dependent differences in COX-related metabolites in genetically modified mice that produce a cyclooxygenase-2 (COX2) enzyme containing a tyrosine 385 to phenylalanine (Y385F) mutation. This mutation renders the COX2 enzyme unable to form a key intermediate radical required
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8

Cherney, David Z. I., James W. Scholey, Rania Nasrallah, et al. "Renal hemodynamic effect of cyclooxygenase 2 inhibition in young men and women with uncomplicated type 1 diabetes mellitus." American Journal of Physiology-Renal Physiology 294, no. 6 (2008): F1336—F1341. http://dx.doi.org/10.1152/ajprenal.00574.2007.

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In experimental studies, cyclooxygenase 2 (COX2)-derived vasodilatory prostaglandins play a more prominent role in arterial vasoregulation in females. The gender-dependent effect of COX2 modulation in humans with type 1 diabetes mellitus (DM) is unknown. Accordingly, we examined the renal hemodynamic role of prostaglandins by assessing the response to COX2 inhibition in young men and women with type 1 DM. We also used a graded ANG II infusion to determine whether gender-based differences were mediated by effects of COX2 inhibition on the renin angiotensin system (RAS). We hypothesized that COX
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9

Stefanski, Casey D., Daniel A. Erkes, Timothy J. Purwin, et al. "Abstract A023: Arachidonic acid metabolism promoting cross resistance in melanoma cells." Cancer Research 84, no. 22_Supplement (2024): A023. http://dx.doi.org/10.1158/1538-7445.tumbody-a023.

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Abstract Melanoma patients initially respond well to first line immunotherapy. However, cross resistance to immunotherapy and BRAF/MEK inhibitor is a clinical challenge for melanoma care. To investigate drug tolerant and resistant mechanisms promoting cross resistance, we analyzed RNA-sequencing and gene set enrichment targeted therapy resistant melanoma cells revealing an enriched arachidonic acid gene signature. Intracellular arachidonic acid levels were increased in drug resistant and drug tolerant melanoma models. Arachidonic acid is enzymatically converted by COX1 and COX2 to prostaglandi
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10

Park, James L., Liming Shu та James A. Shayman. "Differential involvement of COX1 and COX2 in the vasculopathy associated with the α-galactosidase A-knockout mouse". American Journal of Physiology-Heart and Circulatory Physiology 296, № 4 (2009): H1133—H1140. http://dx.doi.org/10.1152/ajpheart.00929.2008.

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The lysosomal storage disorder Fabry disease is characterized by excessive globotriaosylceramide (Gb3) accumulation in major organs such as the heart and kidney. Defective lysosomal α-galactosidase A (Gla) is responsible for excessive Gb3 accumulation, and one cell sensitive to the effects of Gb3 accumulation is vascular endothelium. Endothelial dysfunction is associated with Fabry disease and excessive cellular Gb3. We previously demonstrated that excessive vascular Gb3 in a mouse model of Fabry disease, the Gla-knockout ( Gla−/0) mouse, results in abnormal vascular function, which includes a
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11

Wang, XingJia, Matthew T. Dyson, Youngah Jo, and Douglas M. Stocco. "Inhibition of Cyclooxygenase-2 Activity Enhances Steroidogenesis and Steroidogenic Acute Regulatory Gene Expression in MA-10 Mouse Leydig Cells." Endocrinology 144, no. 8 (2003): 3368–75. http://dx.doi.org/10.1210/en.2002-0081.

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Abstract To study the mechanism for the regulatory effect of arachidonic acid (AA) on steroidogenesis, the role of cyclooxygenase (COX) in steroid production and steroidogenic acute regulatory (StAR) gene expression was investigated. Although stimulation with 0.05 mm dibutyryl cAMP (Bt2cAMP) did not increase StAR protein or progesterone in MA-10 mouse Leydig cells, the addition of 1 μm of the COX inhibitor indomethacin increased StAR protein expression and progesterone production by 5.7-fold and 34.3-fold, respectively. In the presence of indomethacin, the level of Bt2cAMP required for maximal
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12

Wu, Ziyu, Dan Li, Dingyuan Tian, Xuejun Liu, and Zhongming Wu. "Aspirin mediates protection from diabetic kidney disease by inducing ferroptosis inhibition." PLOS ONE 17, no. 12 (2022): e0279010. http://dx.doi.org/10.1371/journal.pone.0279010.

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Diabetic kidney disease (DKD) progression can be predicted by abnormalities in the tubulointerstitial lining, and their treatment may be useful for preventing the disease. DKD is a progressive disease that contributes to renal tubular cell death, but its underlying mechanisms remain unclear. Ferroptosis is a novel term linked to lipid hydroperoxidation, and it plays an important role in the pathogenesis of DKD. Overexpression of cyclooxygenase-2 (COX2), an enzyme of the proximal tubule, causes cellular redox damage in DKD. It remains unknown whether COX2 exacerbates tubular damage by accelerat
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13

Sun, Xiao, Ye Chun Ruan, Jinghui Guo, et al. "Regulation of miR-101/miR-199a-3p by the epithelial sodium channel during embryo implantation: involvement of CREB phosphorylation." REPRODUCTION 148, no. 6 (2014): 559–68. http://dx.doi.org/10.1530/rep-14-0386.

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In our previous study, we have demonstrated that the epithelial sodium channel (ENaC) mediates the embryo-derived signals leading to the activation of CREB and upregulation of cyclooxygenase type 2 (COX2) required for embryo implantation. This study aims to investigate whether microRNAs (miRNAs) are involved in the ENaC-induced upregulation of COX2 during embryo implantation. The results show that the levels of miR-101 and miR-199a-3p, two COX2 targeting miRNAs, are reduced by ENaC activation, and increased by ENaC inhibition or knock-down of ENaC subunit (ENaCα) in human endometrial surface e
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14

Bortolanza, Mariza, Fernando E. Padovan-Neto, Roberta Cavalcanti-Kiwiatkoski, et al. "Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by l -DOPA?" Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1672 (2015): 20140190. http://dx.doi.org/10.1098/rstb.2014.0190.

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Inflammatory mechanisms are proposed to play a role in l -DOPA-induced dyskinesia. Cyclooxygenase-2 (COX2) contributes to inflammation pathways in the periphery and is constitutively expressed in the central nervous system. Considering that inhibition of nitric oxide (NO) formation attenuates l -DOPA-induced dyskinesia, this study aimed at investigating if a NO synthase (NOS) inhibitor would change COX2 brain expression in animals with l -DOPA-induced dyskinesia. To this aim, male Wistar rats received unilateral 6-hydroxydopamine microinjection into the medial forebrain bundle were treated dai
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15

Krieger, Nancy S., and David A. Bushinsky. "Pharmacological inhibition of intracellular calcium release blocks acid-induced bone resorption." American Journal of Physiology-Renal Physiology 300, no. 1 (2011): F91—F97. http://dx.doi.org/10.1152/ajprenal.00276.2010.

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In vivo chronic metabolic acidosis induces net Ca2+ efflux from bone, and incubation of neonatal mouse calvariae in medium simulating physiological metabolic acidosis induces bone resorption. It appears that activation of the proton (H+) receptor OGR1 in the osteoblast leads to an increase in intracellular Ca2+, which is associated with an increase in cyclooxygenase 2 (COX2) and PGE2-induced receptor activator of NF-κB ligand (RANKL) and H+-induced osteoclastic bone resorption. To support this hypothesis, we tested whether intracellular Ca2+ signaling was integral to H+-induced bone resorption
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Wang, Ronghua, Christof Kaltenmeier, Ruiqi Yang, et al. "Abstract 4456: Inducible nitric oxide synthase (iNOS) and cycloxygenase-2 (COX2) inhibition reprogram the tumor microenvironment and suppress tumor growth in hepatocellular carcinoma." Cancer Research 83, no. 7_Supplement (2023): 4456. http://dx.doi.org/10.1158/1538-7445.am2023-4456.

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Abstract Hepatocellular carcinoma is a common cancer worldwide and a leading cause of cancer-related death. Chronic inflammation, accumulation of genetic changes and alternations of the liver microenvironment are critical during the process of carcinogenesis and development of HCC. Inducible nitric oxide synthase (iNOS or NOS2)-derived NO and cyclooxygenase-2 (COX2) are important parts of the neoplastic inflammatory environment. Continuous exposure to moderate to high concentrations of NO, produced by inducible NO synthase (iNOS) and COX2, promotes neoplastic transformation, chemotherapeutic r
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Nguyen, Thanh-Trung, Srilakshmi Nallapaty, G. S. N. Koteswara Rao, Sree Teja Koneru, Satya Sowbhagya Priya Annam, and Vinay Bharadwaj Tatipamula. "Evaluating the In Vitro Activity of Depsidones from Usnea subfloridana Stirton as Key Enzymes Involved in Inflammation and Gout." Pharmaceutical Sciences 27, no. 2 (2020): 291–96. http://dx.doi.org/10.34172/ps.2020.73.

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Background: Traditionally, Usnea genus has significant uses in the treatment of swelling and tumors in Africa and Asia. The aim of the present study was to investigate the chemical constituents present in the acetone extract (AE) of Usnea subfloridana Stirton and also to evaluate their anti-inflammatory and anti-gout effects. Methods: Isolation and characterization of secondary metabolites from AE were evaluated by chromatography and spectral studies. Anti-inflammatory activities were assessed through cyclooxygenase (COX1 and COX2) and 5-lipooxygenase (5-LOX) enzyme inhibition assays, while an
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Vipul, Dubey, and Dil Subba. "A Comparative Study of a Curcumin, Mesalazine and a Cox-2 Inhibitors as a Therapeutic Agents for Ulcerative Colitis by Using A Swiss-Dock Model." Journal of Advancement in Immunology 2, no. 1 (2025): 18–37. https://doi.org/10.5281/zenodo.15332519.

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<em>Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by immune activation, leading to persistent inflammation and tissue damage in the colon. The Janus kinase 1 (COX2) pathway plays a pivotal role in cytokine-mediated immune responses, making it a crucial therapeutic target for UC management.. This study investigates the potential of a Curcumin-Mesalazine combination as a COX2 inhibitor using SwissDock molecular docking simulations. Curcumin, a natural polyphenol derived from Curcuma longa, possesses anti-inflammatory, antioxidant, and immunomodulatory proper
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Wirrig, Elaine E., M. Victoria Gomez, Robert B. Hinton, and Katherine E. Yutzey. "COX2 Inhibition Reduces Aortic Valve Calcification In Vivo." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 4 (2015): 938–47. http://dx.doi.org/10.1161/atvbaha.114.305159.

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Wang, XingJia, Chwan-Li Shen, Matthew T. Dyson, et al. "Cyclooxygenase-2 Regulation of the Age-Related Decline in Testosterone Biosynthesis." Endocrinology 146, no. 10 (2005): 4202–8. http://dx.doi.org/10.1210/en.2005-0298.

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The age-related decline in testosterone biosynthesis in testicular Leydig cells has been well documented, but the mechanisms involved in the decline are not clear. Recent studies have described a cyclooxygenase-2 (COX2)-dependent tonic inhibition of Leydig cell steroidogenesis and expression of the steroidogenic acute regulatory protein (StAR). The present study was conducted to determine whether COX2 protein increases with age in rat Leydig cells and whether COX2 plays a role in the age-related decline in testosterone biosynthesis. Our results indicate that from 3 months of age to 30 months,
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Lim, Sung-Chul, Hyoin Hwang, and Song Iy Han. "Ellagic Acid Inhibits Extracellular Acidity-Induced Invasiveness and Expression of COX1, COX2, Snail, Twist 1, and c-myc in Gastric Carcinoma Cells." Nutrients 11, no. 12 (2019): 3023. http://dx.doi.org/10.3390/nu11123023.

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Extracellular acidity has been implicated in enhanced malignancy and metastatic features in various cancer cells. Gastric cancer cell lines (AGS and SNU601) maintained in an acidic medium have increased motility and invasiveness. In this study, we investigated the effect of ellagic acid, a plant-derived phenolic compound, on the acidity-promoted migration and invasion of gastric cancer cells. Treating cells maintained in acidic medium with ellagic acid inhibited acidity-mediated migration and invasion, and reduced the expression of MMP7 and MMP9. Examining regulatory factors contributing to th
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Cumaoğlu, Ahmet, та Mükerrem Betül Yerer. "The Effects of Aldose Reductase Inhibitor Quercetin and Monochloropivaloylquercetin in Amyloid β Peptide (1–42) Induced Neuroinflammation in Microglial Cells". Natural Product Communications 13, № 6 (2018): 1934578X1801300. http://dx.doi.org/10.1177/1934578x1801300611.

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Microglial over-activation plays a crucial roles during neuroinflammation. Aldose reductase (AR) is one of the enzymes that has been linked to inflammatory processes in several diseases. Therefore, inhibition of AR is considered as an important strategy to reduce inflammation. In the present study, Quercetin (Q) and monochloropivaloylquercetin (MCPQ) showed potent inhibition on AR expression and anti-neuroinflammatory effects in Amyloid β (Aβ) peptide (1–42) induced inflammatory process by inhibiting expression of inflammatory mediators from microglial cells. Furthermore, ablation of AR caused
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Wang, XingJia, Xiangling Yin, Randolph B. Schiffer, Steven R. King, Douglas M. Stocco, and Paula Grammas. "Inhibition of Thromboxane A Synthase Activity Enhances Steroidogenesis and Steroidogenic Acute Regulatory Gene Expression in MA-10 Mouse Leydig Cells." Endocrinology 149, no. 2 (2007): 851–57. http://dx.doi.org/10.1210/en.2007-0470.

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The cyclooxygenase-2 (COX2)-dependent inhibition of Leydig cell steroidogenesis has been demonstrated. To understand the mechanism for this effect of COX2, the present study examined the role of an enzyme downstream of COX2, namely thromboxane A synthase (TBXAS), in steroidogenesis. Inhibition of TBXAS activity with the inhibitor furegrelate induced a concentration-dependent increase in cAMP-induced steroidogenic acute regulatory (StAR) protein in MA-10 mouse Leydig cells. The increase in StAR protein occurred concomitantly with a significant increase in steroid hormone production. Similar res
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Reverte, Virginia, Antonio Tapia, Juan Manuel Moreno, et al. "Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development." American Journal of Physiology-Renal Physiology 301, no. 2 (2011): F327—F333. http://dx.doi.org/10.1152/ajprenal.00110.2011.

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Cyclooxygenase 2 (COX2) is involved in regulating renal hemodynamics after renal ablation. It is also known that high protein intake (HPI) leads to a deterioration of renal function when there is preexisting renal disease and that there are important gender differences in the regulation of renal function. This study tested the hypothesis that the role of COX2 in regulating renal function and the renal hemodynamic effects elicited by HPI are enhanced when nephrogenesis is altered during renal development. It was also expected that the role of COX2 and the effects elicited by HPI are age and sex
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Li, Xiao-Hong, Kristine C. Y. McGrath, Van H. Tran, et al. "Attenuation of Proinflammatory Responses byS-[6]-Gingerol via Inhibition of ROS/NF-Kappa B/COX2 Activation in HuH7 Cells." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/146142.

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Introduction. Hepatic inflammation underlies the pathogenesis of chronic diseases such as insulin resistance and type 2 diabetes mellitus.S-[6]-Gingerol has been shown to have anti-inflammatory properties. Important inflammatory mediators of interleukins include nuclear factorκB (NFκB) and cyclooxygenase 2 (COX2). We now explore the mechanism of anti-inflammatory effects ofS-[6]-gingerol in liver cells.Methods. HuH7 cells were stimulated with IL1βto establish anin vitrohepatic inflammatory model.Results.S-[6]-Gingerol attenuated IL1β-induced inflammation and oxidative stress in HuH7 cells, as
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Basudhar, Debashree, Sharon A. Glynn, Madison Greer, et al. "Coexpression of NOS2 and COX2 accelerates tumor growth and reduces survival in estrogen receptor-negative breast cancer." Proceedings of the National Academy of Sciences 114, no. 49 (2017): 13030–35. http://dx.doi.org/10.1073/pnas.1709119114.

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Proinflammatory signaling pathways are commonly up-regulated in breast cancer. In estrogen receptor-negative (ER−) and triple-negative breast cancer (TNBC), nitric oxide synthase-2 (NOS2) and cyclooxygenase-2 (COX2) have been described as independent predictors of disease outcome. We further explore these findings by investigating the impact of their coexpression on breast cancer survival. Elevated coexpression of NOS2/COX2 proteins is a strong predictor of poor survival among ER− patients (hazard ratio: 21). Furthermore, we found that the key products of NOS2 and COX2, NO and prostaglandin E2
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Yuhas, Yael, Shai Ashkenazi, Eva Berent, and Abraham Weizman. "Clozapine Suppresses the Gene Expression and the Production of Cytokines and Up-Regulates Cyclooxygenase 2 mRNA in Human Astroglial Cells." Brain Sciences 12, no. 12 (2022): 1703. http://dx.doi.org/10.3390/brainsci12121703.

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Schizophrenia (SCZ) is a chronic neurodevelopmental psychotic disorder. The immune system and neuroinflammation seem to play a central role in the pathophysiology of SCZ. Clozapine is an effective atypical antipsychotic used for treatment-resistant SCZ. Life-threatening side effects, such as myocarditis, limit its use. We investigated the immunomodulatory effects of clozapine in an astroglial model of neuroinflammation. We thus assessed the effect of clozapine on the production of inflammatory mediators in human-derived astroglial (A172) cells, stimulated with a cytokine mix (TNFα, IL-1β, IFNγ
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Drif, Assia I., Bharathi Avula, Ikhlas A. Khan, and Thomas Efferth. "COX2-Inhibitory and Cytotoxic Activities of Phytoconstituents of Matricaria chamomilla L." Applied Sciences 13, no. 15 (2023): 8935. http://dx.doi.org/10.3390/app13158935.

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Chamomile tea is a popular beverage and herbal remedy with various health benefits, including antioxidant and antimicrobial activities and beneficial effects on metabolism. In this study, we investigated the inhibitory activities of secondary metabolites from Matricaria chamomile L. against COX2, an enzyme involved in inflammation and linked to cancer development. The cytotoxicity of the compounds was also evaluated on a panel of 60 cancer cell lines. Myricetin, one of the COX2-inhibiting and cytotoxic compounds in chamomile tea, was further studied to determine a proteomic expression profile
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Hu, Chang, Yi, et al. "CCN2 Mediates S1P-Induced Upregulation of COX2 Expression in Human Granulosa-Lutein Cells." Cells 8, no. 11 (2019): 1445. http://dx.doi.org/10.3390/cells8111445.

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CCN1 and CCN2 are members of the CCN family and play essential roles in the regulation of multiple female reproductive functions, including ovulation. Cyclooxygenase-2 (COX2) is a critical mediator of ovulation and can be induced by sphingosine-1-phosphate (S1P) through the S1P1/3-mediated Yes-associated protein (YAP) signaling. However, it is unclear whether CCN1 or CCN2 can mediate S1P-induced upregulation of COX2 expression and increase in prostaglandin E2 (PGE2) production in human granulosa-lutein (hGL) cells. In the present study, we investigated the effects of S1P on the expressions of
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Qi, Jie, Qichao Wu, Qian Cheng, Xiangyuan Chen, Minmin Zhu, and Changhong Miao. "High Glucose Induces Endothelial COX2 and iNOS Expression via Inhibition of Monomethyltransferase SETD8 Expression." Journal of Diabetes Research 2020 (February 24, 2020): 1–10. http://dx.doi.org/10.1155/2020/2308520.

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Cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) overexpression results in endothelial apoptosis, thus mediating vascular endothelial injury in hyperglycaemia. E26 transformation-specific sequence transcription factor-1 (ESE-1), which belongs to the E26 transformation-specific family of transcription factors, has been demonstrated to be involved in COX2 and iNOS gene transcription. Our previous study indicated that SET domain-containing protein 8 (SETD8) downregulation is involved in high glucose-mediated endothelial inflammation in human umbilical vein endothelial cells (HUV
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Deis, Jessica, Te-Yueh Lin, Theresa Bushman, and Xiaoli Chen. "Lipocalin 2 Deficiency Alters Prostaglandin Biosynthesis and mTOR Signaling Regulation of Thermogenesis and Lipid Metabolism in Adipocytes." Cells 11, no. 9 (2022): 1535. http://dx.doi.org/10.3390/cells11091535.

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Apart from a well-known role in the innate immune system, lipocalin 2 (Lcn2) has been recently characterized as a critical regulator of thermogenesis and lipid metabolism. However, the physiological mechanism through which Lcn2 regulates cellular metabolism and thermogenesis in adipocytes remains unknown. We found that Lcn2 expression and secretion are significantly upregulated by arachidonic acid (AA) and mTORC1 inhibition in differentiated inguinal adipocytes. AA-induced Lcn2 expression and secretion correlate with the inflammatory NFkB activation. Lcn2 deficiency leads to the upregulation o
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Pi, Chenyu, Ping Jing, Bingyu Li, et al. "Reversing PD-1 Resistance in B16F10 Cells and Recovering Tumour Immunity Using a COX2 Inhibitor." Cancers 14, no. 17 (2022): 4134. http://dx.doi.org/10.3390/cancers14174134.

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Immunotherapy is an effective method for tumour treatment. Anti-programmed cell death protein 1 (PD-1) and anti-programmed death-ligand 1 (PD-L1) monoclonal antibodies play a significant role in immunotherapy of most tumours; however, some patients develop drug resistance to PD-1/PD-L1 therapy. Cyclooxygenase-2 (COX2) is expressed in various solid tumours, and prostaglandin E2 (PGE2) drives the development of malignant tumours. We developed a drug-resistant B16F10 (B16F10-R) tumour mouse model through four rounds of selection in vivo. Subsequently, we investigated changes in PD-L1 expression a
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Siddique, Abu Bakar, Phillip C. S. R. Kilgore, Afsana Tajmim, et al. "(−)-Oleocanthal as a Dual c-MET-COX2 Inhibitor for the Control of Lung Cancer." Nutrients 12, no. 6 (2020): 1749. http://dx.doi.org/10.3390/nu12061749.

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Lung cancer (LC) represents the topmost mortality-causing cancer in the U.S. LC patients have overall poor survival rate with limited available treatment options. Dysregulation of the mesenchymal epithelial transition factor (c-MET) and cyclooxygenase 2 (COX2) initiates aggressive LC profile in a subset of patients. The Mediterranean extra-virgin olive oil (EVOO)-rich diet already documented to reduce multiple malignancies incidence. (-)-Oleocanthal (OC) is a naturally occurring phenolic secoiridoid exclusively occurring in EVOO and showed documented anti-breast and other cancer activities via
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Zheng, Weiran, Meng Li, Yongxiang Wang, et al. "Guizhi Fuling Capsule Exhibits Antidysmenorrhea Activity by Inhibition of Cyclooxygenase Activity." Evidence-Based Complementary and Alternative Medicine 2020 (May 23, 2020): 1–10. http://dx.doi.org/10.1155/2020/8607931.

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Guizhi Fuling capsule (GZFLc) is a modern preparation from traditional Chinese Medicine. Guizhi Fuling was first prescribed by Zhang Zhongjing almost two thousand years ago for the treatment of primary dysmenorrhea. It has also been used to treat uterine fibroids, dysfunctional uterine bleeding, and endometriosis. Although effective against dysmenorrhea clinically, there are limited information on the mechanism of its action. The major components responsible for the activity are not well defined. The aim of this study has been to elucidate a mechanism that may facilitate the development of a b
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35

Chalabi, M., M. Van Leerdam, A. Aalbers, et al. "Nivolumab, ipilimumab and COX2-inhibition in early stage colon cancer." Annals of Oncology 28 (September 2017): v207. http://dx.doi.org/10.1093/annonc/mdx393.136.

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Yu, Ying, Jinjin Fan, Xin-Sheng Chen, et al. "Genetic model of selective COX2 inhibition reveals novel heterodimer signaling." Nature Medicine 12, no. 6 (2006): 699–704. http://dx.doi.org/10.1038/nm1412.

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37

Sole, Katherine. "Extent of COX2 inhibition might indicate level of cardiovascular risk." Nature Clinical Practice Rheumatology 2, no. 4 (2006): 177. http://dx.doi.org/10.1038/ncprheum0120.

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38

Rose, Tyler M., Christopher A. Reilly, Cassandra E. Deering-Rice, Clinton Brewster, and Chelsea Brewster. "Inhibition of FAAH, TRPV1, and COX2 by NSAID–serotonin conjugates." Bioorganic & Medicinal Chemistry Letters 24, no. 24 (2014): 5695–98. http://dx.doi.org/10.1016/j.bmcl.2014.10.064.

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39

Krishnaswamy, Narayanan, Ghislain Danyod, Pierre Chapdelaine та Michel A. Fortier. "Oxytocin Receptor Down-Regulation Is Not Necessary for Reducing Oxytocin-Induced Prostaglandin F2α Accumulation by Interferon-τ in a Bovine Endometrial Epithelial Cell Line". Endocrinology 150, № 2 (2009): 897–905. http://dx.doi.org/10.1210/en.2008-0704.

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Interferon-τ (IFNτ) is the embryonic signal responsible for pregnancy recognition in ruminants. The primary action of IFNτ is believed to be mediated through inhibition of prostaglandin F2α (PGF2α) released from the endometrial epithelial cells in response to oxytocin (OT). Our working hypothesis was that the antiluteolytic effect of IFNτ also involved modulation of PG production downstream of OT receptor (OTR) and/or cyclooxygenase 2 (COX2). There is currently no OT-sensitive endometrial cell line to study the molecular mechanisms underlying our hypotheses. Therefore, we established an immort
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Ferreira, Matthew Thomas, Juliano Andreoli Miyake, Renata Nascimento Gomes, et al. "Cyclooxygenase Inhibition Alters Proliferative, Migratory, and Invasive Properties of Human Glioblastoma Cells In Vitro." International Journal of Molecular Sciences 22, no. 9 (2021): 4297. http://dx.doi.org/10.3390/ijms22094297.

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Prostaglandin E2 (PGE2) is known to increase glioblastoma (GBM) cell proliferation and migration while cyclooxygenase (COX) inhibition decreases proliferation and migration. The present study investigated the effects of COX inhibitors and PGE2 receptor antagonists on GBM cell biology. Cells were grown with inhibitors and dose response, viable cell counting, flow cytometry, cell migration, gene expression, Western blotting, and gelatin zymography studies were performed. The stimulatory effects of PGE2 and the inhibitory effects of ibuprofen (IBP) were confirmed in GBM cells. The EP2 and EP4 rec
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Serrano-Sanchez, Martin, Zahra Tanfin, and Denis Leiber. "Signaling Pathways Involved in Sphingosine Kinase Activation and Sphingosine-1-Phosphate Release in Rat Myometrium in Late Pregnancy: Role in the Induction of Cyclooxygenase 2." Endocrinology 149, no. 9 (2008): 4669–79. http://dx.doi.org/10.1210/en.2008-1756.

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We investigated the regulation of the sphingosine kinase (SphK)/sphingosine-1-phosphate (S1P) axis and its role during pregnancy in the rat myometrium. SphK1 and SphK2 were coexpressed in myometrium during gestation. The levels and activity of SphK1/2 were modest at midgestation (d 12), increased at d 19 and progressively declined to low at postpartum. Similar patterns were observed for the phosphorylation of ERK and protein kinase C (PKC). Inhibition of PKC and ERK reduced SphK1/2 activity. In late pregnancy, levels of cyclooxygenase 2 (COX2) increased in parallel to SphK levels. Using a phar
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Reverte, Virginia, Antonio Tapia, Analia Loria, Francisco Salazar, M. Teresa Llinas, and F. Javier Salazar. "COX2 inhibition during nephrogenic period induces ANG II hypertension and sex-dependent changes in renal function during aging." American Journal of Physiology-Renal Physiology 306, no. 5 (2014): F534—F541. http://dx.doi.org/10.1152/ajprenal.00535.2013.

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This study was performed to test the hypothesis that ANG II contributes to the hypertension and renal functional alterations induced by a decrease of COX2 activity during the nephrogenic period. It was also examined whether renal functional reserve and renal response to volume overload and high sodium intake are reduced in 3–4- and 9–11-mo-old male and female rats treated with vehicle or a COX2 inhibitor during nephrogenic period (COX2np). Our data show that this COX2 inhibition induces an ANG II-dependent hypertension that is similar in male and female rats. Renal functional reserve is reduce
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Lee, Hye Sun, Sung Ji Yun, Jung Min Ha, et al. "Prostaglandin D2 stimulates phenotypic changes in vascular smooth muscle cells." Experimental & Molecular Medicine 51, no. 11 (2019): 1–10. http://dx.doi.org/10.1038/s12276-019-0330-3.

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AbstractSince chronic inflammation is associated with the pathogenesis of atherosclerosis, inflammatory cytokines might contribute to the phenotypic modulation of vascular smooth muscle cells (VSMCs). Tumor necrosis factor α (TNFα) facilitated the transformation of contractile VSMCs to the synthetic phenotype, as determined by the expression of marker proteins and a collagen gel contraction assay. Western blot analysis and a cyclooxygenase-2 (COX2) promoter assay revealed that TNFα stimulation resulted in the induction of COX2. The overexpression, silencing, or pharmacological inhibition of CO
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Liu, Sisi, Emmanouil Saloustros, Annabel Berthon, et al. "Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia." Endocrine-Related Cancer 23, no. 1 (2015): 15–25. http://dx.doi.org/10.1530/erc-15-0472.

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Primary pigmented nodular adrenocortical disease (PPNAD), whether in the context of Carney complex (CNC) or isolated, leads to ACTH-independent Cushing's syndrome (CS). CNC and PPNAD are caused typically by inactivating mutations of PRKAR1A, a gene coding for the type 1a regulatory subunit (R1α) of cAMP-dependent protein kinase (PKA). Mice lacking Prkar1a, specifically in the adrenal cortex (AdKO) developed CS caused by bilateral adrenal hyperplasia (BAH), which is formed from the abnormal proliferation of fetal-like adrenocortical cells. Celecoxib is a cyclooxygenase 2 (COX2) inhibitor. In bo
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CROXTALL, Jamie D., Mark PAUL-CLARK, and Peter Th W. van HAL. "Differential modulation of glucocorticoid action by FK506 in A549 cells." Biochemical Journal 376, no. 1 (2003): 285–90. http://dx.doi.org/10.1042/bj20030821.

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Glucocorticoids inhibit the release of eicosanoid pro-inflammatory mediators. The immunosuppressant FK506 is known to enhance many aspects of glucocorticoid action. In the present study we show that FK506 (1 μM or 10 μM) inhibits the release of arachidonic acid and prostaglandin E2 from A549 cells and also inhibits their proliferation. Simultaneous treatment of FK506 together with the glucocorticoids dexamethasone, methyl-prednisolone, fluticasone or mometasone (10 nM) enhances the growth inhibitory effect of these steroids. Furthermore, the simultaneous use of FK506 and these glucocorticoids
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Agarwal, V., M. J. Lind, and L. Cawkwell. "66 Inhibition of EGFR, MTOR and COX2 pathways in mesothelioma cells." Lung Cancer 75 (January 2012): S22. http://dx.doi.org/10.1016/s0169-5002(12)70067-3.

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47

Xiao, Jingzhe, Chunyan Xu, Rongxin Zhu, Pengyu Fu, Jie Jia та Lijing Gong. "Exercise Improves the Cytoskeletal and Metabolic Functions of Brown Adipocytes Through the ADRβ3/COX2-Ywhah Axis". International Journal of Molecular Sciences 26, № 7 (2025): 2978. https://doi.org/10.3390/ijms26072978.

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Brown adipose tissue (BAT) is a critical target for obesity treatment, and exercise can enhance BAT function through the activation of ADRβ3. However, the molecular mechanisms underlying BAT metabolism following the exercise-induced activation of ADRβ3 remain unclear. This study utilized RNA sequencing, Western blotting, Oil Red O staining, weighted gene co-expression network analysis (WGCNA), and machine learning to investigate the role of the ADRβ3-COX2 pathway in lipid metabolism in brown adipocytes. We identified Ywhah as a key gene and validated our findings using external datasets. Our r
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Qiang, Ya-Wei, Shiqiao Ye, Yu Chen, et al. "Mutant KRAS Enhances Stress Granules and Resistance to Proteasome Inhibition Via 15-d-PGJ2 in Multiple Myeloma." Blood 134, Supplement_1 (2019): 4383. http://dx.doi.org/10.1182/blood-2019-130493.

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Introduction: Mutant KRAS leads to activation of the MEK/ERK pathway in approximately 20% of multiple myeloma (MM) patients. Stress granules (SGs) are cytosolic non-membranous structures composed of translational mRNAs, ribosomal proteins, and RNA-binding proteins, which form in response to different stress stimuli and chemotherapeutic treatment. We have previously shown that mutant KRAS upregulates SG formation. The molecular mechanisms underlying this process are unclear. The purpose of this study was to elucidate a) the mechanism by which mutant KRAS upregulates SG formation and b) to provi
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Prima, Victor, Lyudmila N. Kaliberova, Sergey Kaliberov, David T. Curiel, and Sergei Kusmartsev. "COX2/mPGES1/PGE2pathway regulates PD-L1 expression in tumor-associated macrophages and myeloid-derived suppressor cells." Proceedings of the National Academy of Sciences 114, no. 5 (2017): 1117–22. http://dx.doi.org/10.1073/pnas.1612920114.

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In recent years, it has been established that programmed cell death protein ligand 1 (PD-L1)–mediated inhibition of activated PD-1+T lymphocytes plays a major role in tumor escape from immune system during cancer progression. Lately, the anti–PD-L1 and –PD-1 immune therapies have become an important tool for treatment of advanced human cancers, including bladder cancer. However, the underlying mechanisms of PD-L1 expression in cancer are not fully understood. We found that coculture of murine bone marrow cells with bladder tumor cells promoted strong expression of PD-L1 in bone marrow–derived
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Stables, Melanie J., Justine Newson, Samir S. Ayoub, Jeremy Brown, Catherine J. Hyams, and Derek W. Gilroy. "Priming innate immune responses to infection by cyclooxygenase inhibition kills antibiotic-susceptible and -resistant bacteria." Blood 116, no. 16 (2010): 2950–59. http://dx.doi.org/10.1182/blood-2010-05-284844.

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AbstractInhibition of cyclooxygenase (COX)–derived prostaglandins (PGs) by nonsteroidal anti-inflammatory drugs (NSAIDs) mediates leukocyte killing of bacteria. However, the relative contribution of COX1 versus COX2 to this process, as well as the mechanisms controlling it in mouse and humans, are unknown. Indeed, the potential of NSAIDs to facilitate leukocyte killing of drug-resistant bacteria warrants investigation. Therefore, we carried out a series of experiments in mice and humans, finding that COX1 is the predominant isoform active in PG synthesis during infection and that its prophylac
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