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Journal articles on the topic 'In vitro hepatic systems'

Author: Grafiati

Published: 10 September 2021

Last updated: 29 July 2025

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1

Chang, Ming-Ling, and Sien-Sing Yang. "Metabolic Signature of Hepatic Fibrosis: From Individual Pathways to Systems Biology." Cells 8, no. 11 (2019): 1423. http://dx.doi.org/10.3390/cells8111423.

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Hepatic fibrosis is a major cause of morbidity and mortality worldwide, as it ultimately leads to cirrhosis, which is estimated to affect up to 2% of the global population. Hepatic fibrosis is confirmed by liver biopsy, and the erroneous nature of this technique necessitates the search for noninvasive alternatives. However, current biomarker algorithms for hepatic fibrosis have many limitations. Given that the liver is the largest organ and a major metabolic hub in the body, probing the metabolic signature of hepatic fibrosis holds promise for the discovery of new markers and therapeutic targe

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2

Kiss, Izabella, Nicole Neuwert, Raimund Oberle, Markus Hengstschläger, Selma Osmanagic-Myers, and Herbert Stangl. "Hepatic Lipoprotein Metabolism: Current and Future In Vitro Cell-Based Systems." Biomolecules 15, no. 7 (2025): 956. https://doi.org/10.3390/biom15070956.

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Changes in hepatic lipoprotein metabolism are responsible for the majority of metabolic dysfunction-associated disorders, including familial hypercholesterolemia (FH), metabolic syndrome (MetS), metabolic dysfunction-associated fatty liver disease (MAFLD), and age-related diseases such as atherosclerosis, a major health burden in modern society. This review aims to advance the understanding of state-of-the-art mechanistic concepts in lipoprotein metabolism, with a particular focus on lipoprotein uptake and secretion and their dysregulation in disease, and to provide a comprehensive overview of

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Kammerer, Sarah. "Three-Dimensional Liver Culture Systems to Maintain Primary Hepatic Properties for Toxicological Analysis In Vitro." International Journal of Molecular Sciences 22, no. 19 (2021): 10214. http://dx.doi.org/10.3390/ijms221910214.

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Drug-induced liver injury (DILI) is the major reason for failures in drug development and withdrawal of approved drugs from the market. Two-dimensional cultures of hepatocytes often fail to reliably predict DILI: hepatoma cell lines such as HepG2 do not reflect important primary-like hepatic properties and primary human hepatocytes (pHHs) dedifferentiate quickly in vitro and are, therefore, not suitable for long-term toxicity studies. More predictive liver in vitro models are urgently required in drug development and compound safety evaluation. This review discusses available human hepatic cel

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Miyashita, Hitoshi, Atsushi Suzuki, Katashi Fukao, Hiromitsu Nakauchi, and Hideki Taniguchi. "Evidence for Hepatocyte Differentiation from Embryonic Stem Cells In Vitro." Cell Transplantation 11, no. 5 (2002): 429–34. http://dx.doi.org/10.3727/000000002783985675.

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We confirmed hepatocyte differentiation from embryonic stem (ES) cells in vitro. RT-PCR analysis revealed that a broad range of hepatic gene expression was observed in ES cells differentiated through formation of embryoid bodies (EBs) and its attachment culture. Quantitative PCR analysis revealed that hepatic gene expression related to early and late-stage liver development were enhanced through in vitro differentiation of ES cells. The presence of albumin-producing cells in the peripheral region of attached EBs was confirmed by immunocytochemical analysis. Future experiments will reveal the m

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Bořek-Dohalská, Lucie, та Marie Stiborová. "Cytochrome P450 3A activities and their modulation by α-naphthoflavone in vitro are dictated by the efficiencies of model experimental systems". Collection of Czechoslovak Chemical Communications 75, № 2 (2010): 201–20. http://dx.doi.org/10.1135/cccc2009525.

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The knowledge on efficiencies of different in vitro systems containing cytochromes P450 (CYP) of a 3A subfamily is crucial to screen potential substrates of these CYPs. We evaluated and compared efficiencies of several in vitro CYP3A enzymatic systems to oxidize the model substrates, α-NF and testosterone, under the standardized experimental conditions. Five CYP3A systems were tested: (i) human hepatic microsomes rich in CYP3A4, (ii) hepatic microsomes of rabbits treated with a CYP3A6 inducer, rifampicine, (iii) microsomes of Baculovirus transfected insect cells containing recombinant human CY

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Yun, Jingyeong, Tae-Joon Jeon, and Sun Min Kim. "Current Advances and Future Perspectives of Liver-on-a-Chip Platforms Incorporating Dynamic Fluid Flow." Biomimetics 10, no. 7 (2025): 443. https://doi.org/10.3390/biomimetics10070443.

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The liver is a vital organ responsible for a broad range of metabolic functions, including glucose and lipid metabolism, detoxification, and protein synthesis. Its structural complexity, characterized by hexagonal hepatic lobules composed of diverse parenchymal and non-parenchymal cell types, supports its broad spectrum of physiological activities. Traditional in vitro liver models have contributed significantly to our understanding of hepatic biology and the development of therapies for liver-related diseases. However, static culture systems fail to replicate the dynamic in vivo microenvironm

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Ponsoda, Xavier, Ramiro Jover, José Vicente Castell, and Mariá José Gómez-Lechón. "In Vitro Toxicity to Two Cellular Systems of the First Ten Chemicals on the MEIC List." Alternatives to Laboratory Animals 17, no. 3 (1990): 218–23. http://dx.doi.org/10.1177/026119299001700318.

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The cytotoxic effects of the first 10 chemicals on the MEIC list were evaluated with two experimental cellular systems, monolayer cultures of rat hepatocytes and cell lines (Hep G2 and 3T3). Three endpoints were measured to evaluate cytotoxicity, intracellular LDH activity, cellular protein content and the MTT test. The results show that: 1. digoxin, amitriptyline and diazepam were the most cytotoxic chemicals (IC50:0.01-0.5mM); 2. alcoholic compounds (sopropanol, ethylene glycol, ethanol and methanol) produced the lowest toxic effects (IC50: 100–1500mM); 3. paracetamol, acetylsalicylic acid a

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Ponsoda, Xavier, Cristina Núñez, José Vicente Castell, and Maria José Gómez-Lechón. "Evaluation of the Cytotoxic Effects of MEIC Chemicals 31–50 on Primary Culture of Rat Hepatocytes and Hepatic and Non-hepatic Cell Lines." Alternatives to Laboratory Animals 25, no. 4 (1997): 423–36. http://dx.doi.org/10.1177/026119299702500405.

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The cytotoxicities of 20 chemicals (numbers 31–50) from the Multicenter Evaluation of In Vitro Cytotoxicity (MEIC) programme were assessed with a primary culture of rat hepatocytes and with two hepatic cell lines (Hep G2 and FaO) and one non-hepatic cell line (3T3). The cytotoxicities of the chemicals were evaluated by using the MTT test after the cells had been exposed to the chemicals for 24 hours. For a better evaluation of results, dose–response curves were mathematically linearised and cytotoxicity was expressed as IC50 values and IC10 values (the concentration causing 50% and 10% loss of

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9

Bruscalupi, G., S. Leoni, M. T. Mangiantini, F. Piemonte, S. Spagnuolo, and A. Trentalance. "Short term regulation of acyl CoA: Cholesterol acyl transferase (ACAT) activity in the regenerating and perinatal liver." Bioscience Reports 5, no. 3 (1985): 237–42. http://dx.doi.org/10.1007/bf01119593.

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Acyl coenzyme A:cholesterol acyltransferase (ACAT), the enzyme catalyzing the hepatic cholesterol esterification could be involved in the modified availability of cholesterol detectable in proliferating systems. While no significant variations are detectable in the regenerating liver, the modified ACAT activity during liver development and its differential sensitivity to the in vitro stimulation of modulatory systems suggest an involvement of the enzyme in this proliferating process.

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Hallifax, D., and J. Houston. "Methodological Uncertainty in Quantitative Prediction of Human Hepatic Clearance from In Vitro Experimental Systems." Current Drug Metabolism 10, no. 3 (2009): 307–21. http://dx.doi.org/10.2174/138920009787846341.

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11

Gómez-Lechón, María José, Teresa Donato, Xavier Ponsoda, and José V. Castell. "Human Hepatic Cell Cultures: In Vitro and In Vivo Drug Metabolism." Alternatives to Laboratory Animals 31, no. 3 (2003): 257–65. http://dx.doi.org/10.1177/026119290303100307.

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Drug metabolism is the major determinant of drug clearance, and the factor most frequently responsible for inter-individual differences in drug pharmacokinetics. The expression of drug metabolising enzymes shows significant interspecies differences, and variability among human individuals (polymorphic or inducible enzymes) makes the accurate prediction of the metabolism of a new compound in humans difficult. Several key issues need to be addressed at the early stages of drug development to improve drug candidate selection: a) how fast the compound will be metabolised; b) what metabolites will

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12

Morgan, Katie, Steven D. Morley, Arslan K. Raja, et al. "Metabolism of Acetaminophen by Enteric Epithelial Cells Mitigates Hepatocellular Toxicity In Vitro." Journal of Clinical Medicine 12, no. 12 (2023): 3995. http://dx.doi.org/10.3390/jcm12123995.

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The gut–liver axis is defined by dietary and environmental communication between the gut, microbiome and the liver with its redox and immune systems, the overactivation of which can lead to hepatic injury. We used media preconditioning to mimic some aspects of the enterohepatic circulation by treating the human Caco-2 intestinal epithelial cell line with 5, 10 and 20 mM paracetamol (N-acetyl-para-aminophenol; APAP) for 24 h, after which cell culture supernatants were transferred to differentiated human hepatic HepaRG cells for a further 24 h. Cell viability was assessed by mitochondrial functi

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Nakamura, Masao, Yuriko Uehara, Masahiro Asada, Masashi Suzuki, and Toru Imamura. "Sulfated Glycosaminoglycan-Assisted Receptor Specificity of Human Fibroblast Growth Factor (FGF) 19 Signaling in a Mouse System Is Different from That in a Human System." Journal of Biomolecular Screening 18, no. 3 (2012): 321–30. http://dx.doi.org/10.1177/1087057112463820.

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The endocrine action of human (h) intestine-derived fibroblast growth factor 19 (hFGF19) toward liver cells necessitates a highly specific recognition system. We previously reported that at physiological concentrations (~30 pM), hFGF19 requires sulfated glycosaminoglycans (sGAGs) for its signaling via human FGF receptor 4 (hFGFR4) in the presence of a co-receptor, human βKlotho (hKLB), thus establishing specific targeting. Here we report that the specificity of hFGF19 signaling is greatly altered in a mouse model system. In in vitro cellular systems, at concentrations achievable in transgenic

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14

Jia, Zhidong, Yuan Cheng, Xinan Jiang, et al. "3D Culture System for Liver Tissue Mimicking Hepatic Plates for Improvement of Human Hepatocyte (C3A) Function and Polarity." BioMed Research International 2020 (March 4, 2020): 1–22. http://dx.doi.org/10.1155/2020/6354183.

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In vitro 3D hepatocyte culture constitutes a core aspect of liver tissue engineering. However, conventional 3D cultures are unable to maintain hepatocyte polarity, functional phenotype, or viability. Here, we employed microfluidic chip technology combined with natural alginate hydrogels to construct 3D liver tissues mimicking hepatic plates. We comprehensively evaluated cultured hepatocyte viability, function, and polarity. Transcriptome sequencing was used to analyze changes in hepatocyte polarity pathways. The data indicate that, as culture duration increases, the viability, function, polari

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15

Kuhrt, Heidrun, Michał Walski, Andreas Reichenbach, and Jan Albrecht. "Rabbit retinal organ culture as an in-vitro model of hepatic retinopathy." Graefe's Archive for Clinical and Experimental Ophthalmology 242, no. 6 (2004): 512–22. http://dx.doi.org/10.1007/s00417-004-0882-2.

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Boyer, J. L. "Bile duct epithelium: frontiers in transport physiology." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 1 (1996): G1—G5. http://dx.doi.org/10.1152/ajpgi.1996.270.1.g1.

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The bile duct epithelium is known to modify hepatic bile by both secretory and absorptive processes. However, identification and characterization of the transport systems that carry out these physiological functions at the cellular and molecular level have been slow compared with progress in understanding hepatic bile production. Recently, techniques have been developed that enable bile duct cells to be isolated in substantial number and purity and as intact polarized units that can be studied in vitro. These newer preparations have enabled classic physiological approaches to be performed dire

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Donato, M. Teresa, Gloria Gallego-Ferrer, and Laia Tolosa. "In Vitro Models for Studying Chronic Drug-Induced Liver Injury." International Journal of Molecular Sciences 23, no. 19 (2022): 11428. http://dx.doi.org/10.3390/ijms231911428.

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Drug-induced liver injury (DILI) is a major clinical problem in terms of patient morbidity and mortality, cost to healthcare systems and failure of the development of new drugs. The need for consistent safety strategies capable of identifying a potential toxicity risk early in the drug discovery pipeline is key. Human DILI is poorly predicted in animals, probably due to the well-known interspecies differences in drug metabolism, pharmacokinetics, and toxicity targets. For this reason, distinct cellular models from primary human hepatocytes or hepatoma cell lines cultured as 2D monolayers to em

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Gassaway, Brandon M., Max C. Petersen, Yulia V. Surovtseva та ін. "PKCε contributes to lipid-induced insulin resistance through cross talk with p70S6K and through previously unknown regulators of insulin signaling". Proceedings of the National Academy of Sciences 115, № 38 (2018): E8996—E9005. http://dx.doi.org/10.1073/pnas.1804379115.

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Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C ε (PKCε), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high-fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCε protects against high-fat diet-induced hepatic insulin resistance. Here, we employed a systems-level approach to uncover additional signaling pathways involved in high-fat diet-induced hepatic insulin resistance. We used quantit

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Bhat, Ganesh B., Brian C. W. Hummel, and Paul G. Walfish. "Thioredoxin and glutaredoxin systems of rat liver cytosol are not influenced by thyroid dysfunction." Biochemistry and Cell Biology 67, no. 7 (1989): 384–87. http://dx.doi.org/10.1139/o89-060.

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The relation of thyroid hormone status to the function of hepatic cytosolic components activating microsomal reverse triiodothyronine (rT3) 5′-monodeiodination was studied in rats. Hyperthyroidism was induced by administration of thyroxine and hypothyroidism, by thyroidectomy. The DTT-stimulated microsomal rT3 5′-monodeiodination rate was increased by 125% in hyperthyroid rats and reduced to about 30% in hypothyroid rats (when compared with euthyroid animals). Thyroid status was unrelated to NADPH-dependent activation of microsomal 5′-deiodinase by cytosol components or to cytosolic concentrat

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Cheng, Hsin-Chung, Hsueh-Tien Chen, Hsin-Ying Chen, et al. "Advancing hepatic clearance prediction across in vitro, ex situ, and in vivo systems to facilitate in vitro-to-in vivo extrapolation." European Journal of Pharmaceutical Sciences 212 (September 2025): 107171. https://doi.org/10.1016/j.ejps.2025.107171.

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21

Cotovio, João P., and Tiago G. Fernandes. "Production of Human Pluripotent Stem Cell-Derived Hepatic Cell Lineages and Liver Organoids: Current Status and Potential Applications." Bioengineering 7, no. 2 (2020): 36. http://dx.doi.org/10.3390/bioengineering7020036.

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Liver disease is one of the leading causes of death worldwide, leading to the death of approximately 2 million people per year. Current therapies include orthotopic liver transplantation, however, donor organ shortage remains a great challenge. In addition, the development of novel therapeutics has been limited due to the lack of in vitro models that mimic in vivo liver physiology. Accordingly, hepatic cell lineages derived from human pluripotent stem cells (hPSCs) represent a promising cell source for liver cell therapy, disease modelling, and drug discovery. Moreover, the development of new

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Herrero, Alba, Elisabeth Knetemann, and Inge Mannaerts. "Review: Challenges of In Vitro CAF Modelling in Liver Cancers." Cancers 13, no. 23 (2021): 5914. http://dx.doi.org/10.3390/cancers13235914.

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Primary and secondary liver cancer are the third cause of death in the world, and as the incidence is increasing, liver cancer represents a global health burden. Current treatment strategies are insufficient to permanently cure patients from this devastating disease, and therefore other approaches are under investigation. The importance of cancer-associated fibroblasts (CAFs) in the tumour microenvironment is evident, and many pre-clinical studies have shown increased tumour aggressiveness in the presence of CAFs. However, it remains unclear how hepatic stellate cells are triggered by the tumo

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Schwald, F., J. Velazquez, B. Fischer, et al. "P16-37: Comparative assessment of hepatic in vitro systems for detection of drug-induced liver injury." Toxicology Letters 384 (September 2023): S195. http://dx.doi.org/10.1016/s0378-4274(23)00726-9.

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Niu, Xia, Yanan Meng, Yucheng Wang, and Guiling Li. "Established Liposome-Coated IMB16-4 Polymeric Nanoparticles (LNPs) for Increasing Cellular Uptake and Anti-Fibrotic Effects In Vitro." Molecules 27, no. 12 (2022): 3738. http://dx.doi.org/10.3390/molecules27123738.

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As a global health problem, liver fibrosis still does not have approved treatment. It was proved that N-(3,4,5-trichlorophenyl)-2(3-nitrobenzenesulfonamide) benzamide (IMB16-4) has anti-hepatic fibrosis activity. However, IMB16-4 displays poor water solubility and poor bioavailability. We are devoted to developing biodegraded liposome-coated polymeric nanoparticles (LNPs) as IMB16-4 delivery systems for improving aqueous solubility, cellular uptake, and anti-fibrotic effects. The physical states of IMB16-4−LNPs were analyzed using a transmission electron microscope (TEM), high-performance liqu

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Timchalk, C., and A. K. Charles. "Differential Effects of Carcinogens on Hepatic Cytosolic Cyclic AMP-dependent Protein Kinase Activity." Journal of the American College of Toxicology 5, no. 4 (1986): 267–73. http://dx.doi.org/10.3109/10915818609140751.

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Differential effects of epigenetic tumor promoters and a genotoxic carcinogen on hepatic cytosolic cyclic adenosine 3′,5′-monophosphate-dependent protein kinase (CAMP-PK) were studied in vitro, since this enzyme is one of the major mediators of cell membrane permeability. Mirex (dodecachlorooctahydro-1,3,4-metheno-2H-cyclobuto[cd]pentalene), like phorbol ester TPA (12-0-tetradecanoylphorbol-13-acetste), caused significant inhibition of cAMP-dependent protein kinase activity ratio, whereas DDT [p, p′-trichlorobis(p-chlorophenyl)ethane] produced concentration-dependent changes. Diethylnitrosamin

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Liu, Xunzhi, Changlong Fang, Hongling Yu, et al. "Chondroitin Sulfate-Based Imatinib Nanoparticles Targeting Activated Hepatic Stellate Cells Against Hepatic Fibrosis." Pharmaceutics 17, no. 3 (2025): 351. https://doi.org/10.3390/pharmaceutics17030351.

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Background: Activated hepatic stellate cells (aHSCs) play a significant role during the onset of hepatic fibrosis, ultimately leading to excessive deposition of extracellular matrix (ECM) and other typical pathological features, and thus have become a popular target for the treatment of hepatic fibrosis. However, current aHSC-centric therapy strategies achieve unsatisfactory results, mainly due to the lack of approved anti-fibrosis drugs and sufficiently efficient aHSC-targeted delivery systems. In this study, our aim was to develop an Imatinib-loaded nanoparticle delivery system based on a ch

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Medine, Claire N., Sebastian Greenhough, and David C. Hay. "Role of stem-cell-derived hepatic endoderm in human drug discovery." Biochemical Society Transactions 38, no. 4 (2010): 1033–36. http://dx.doi.org/10.1042/bst0381033.

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Accurate prediction of human drug toxicity is a vital part of the drug discovery process. However, the safety evaluation process is hindered by the availability and quality of primary human liver models with which to study drug toxicity. In an attempt to overcome this limitation, research has focused on deriving human hepatocytes from a number of sources, including progenitors from fetal and adult liver, human cell lines derived from liver tumours, immortalized human hepatocytes and pluripotent stem cells. The major hurdles in developing scalable and high-fidelity human hepatocytes from hepati

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Yang, Ai-Ting, Dou-Dou Hu, Ping Wang та ін. "TGF-β1 Induces the Dual Regulation of Hepatic Progenitor Cells with Both Anti- and Proliver Fibrosis". Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/1492694.

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Transforming growth factor-beta 1 (TGF-β1) plays a central role in hepatic progenitor cells- (HPCs-) mediated liver repair and fibrosis. However, different effects of TGF-β1 on progenitor cells have not been described. In this study, both in vitro (HPCs cocultured with hepatic stellate cells (HSCs) in transwells) and in vivo (CCl4-injured liver fibrosis rat) systems were used to evaluate the impacts. We found that HPCs pretreated with TGF-β1 for 12 hours inhibited the activation of HSCs, while sensitization for 48 hours increased the activation of HSCs. Consistent with these in vitro results,

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Chabin-Brion, Karine, Jérôme Marceiller, Franck Perez, et al. "The Golgi Complex Is a Microtubule-organizing Organelle." Molecular Biology of the Cell 12, no. 7 (2001): 2047–60. http://dx.doi.org/10.1091/mbc.12.7.2047.

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We show that the Golgi complex can directly stimulate microtubule nucleation in vivo and in vitro and thus behaves as a potent microtubule-organizing organelle in interphase cells. With the use of nocodazole wash-out experiments in hepatic cells, we found that the occurrence of noncentrosomal, early stabilized microtubules is highly correlated with the subcellular localization of Golgi membranes. With the use of in vitro reconstituted microtubule assembly systems with or without cytosol, we also found that, in contrast to centrosomally attached microtubules, the distal ends of Golgi-attached m

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Houston, J. Brian, Karen Rowland-Yeo, and Ugo Zanelli. "Evaluation of the novel in vitro systems for hepatic drug clearance and assessment of their predictive utility." Toxicology in Vitro 26, no. 8 (2012): 1265–71. http://dx.doi.org/10.1016/j.tiv.2011.12.016.

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Rodrigues, Robim M., Olivier Govaere, Tania Roskams, Tamara Vanhaecke, Vera Rogiers, and Joery De Kock. "Gene expression data from acetaminophen-induced toxicity in human hepatic in vitro systems and clinical liver samples." Data in Brief 7 (June 2016): 1052–57. http://dx.doi.org/10.1016/j.dib.2016.03.069.

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Howell, Lawrence, Rosalind E. Jenkins, Stephen Lynch, Carrie Duckworth, B. Kevin Park, and Christopher Goldring. "Proteomic profiling of murine biliary-derived hepatic organoids and their capacity for drug disposition, bioactivation and detoxification." Archives of Toxicology 95, no. 7 (2021): 2413–30. http://dx.doi.org/10.1007/s00204-021-03075-3.

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AbstractHepatic organoids are a recent innovation in in vitro modeling. Initial studies suggest that organoids better recapitulate the liver phenotype in vitro compared to pre-existing proliferative cell models. However, their potential for drug metabolism and detoxification remains poorly characterized, and their global proteome has yet to be compared to their tissue of origin. This analysis is urgently needed to determine what gain-of-function this new model may represent for modeling the physiological and toxicological response of the liver to xenobiotics. Global proteomic profiling of undi

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Lebeck, Janne, Muhammad Umar Cheema, Mariusz T. Skowronski, Søren Nielsen та Jeppe Praetorius. "Hepatic AQP9 expression in male rats is reduced in response to PPARα agonist treatment". American Journal of Physiology-Gastrointestinal and Liver Physiology 308, № 3 (2015): G198—G205. http://dx.doi.org/10.1152/ajpgi.00407.2013.

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The peroxisome proliferator receptor α (PPARα) is a key regulator of the hepatic response to fasting with effects on both lipid and carbohydrate metabolism. A role in hepatic glycerol metabolism has also been found; however, the results are somewhat contradictive. Aquaporin 9 (AQP9) is a pore-forming transmembrane protein that facilitates hepatic uptake of glycerol. Its expression is inversely regulated by insulin in male rodents, with increased expression during fasting. Previous results indicate that PPARα plays a crucial role in the induction of AQP9 mRNA during fasting. In the present stud

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Dongsogo, Julius, Christopher Larbie, Abdul Mumeen Idrissu, Ataanya Daniel Abera, and Turrisoe Daniel. "Hepatoprotective Activity of Plant Extracts in Non-Human Models: The Toxicants Solvents and Diseased Models-A Review." American Journal of Multidisciplinary Research and Innovation 2, no. 6 (2023): 49–56. http://dx.doi.org/10.54536/ajmri.v2i6.672.

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The search for an ideal hepatic regenerative agent has led to the modelling of several forms of liver disorders. This involves the usage of various substances in in-vitro and in-vivo systems that are injurious to the human liver in in-vitro and in-vivo systems and then challenged with plants parts extracted with organic and inorganic solvents. Reported view works on hepatotoxicity have been focused on the plant species, this review therefore focused on the toxicants, the solvents for extraction and models used in inducing the hepatotoxicity. Google search, Elsevier and PubMed databases were se

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Krishnan, Preethi, Andrew K. Smith, Glen E. P. Ropella, Lopamudra Dutta, Ryan C. Kennedy, and C. Anthony Hunt. "Utilizing virtual experiments to increase understanding of discrepancies involving in vitro-to-in vivo predictions of hepatic clearance." PLOS ONE 17, no. 7 (2022): e0269775. http://dx.doi.org/10.1371/journal.pone.0269775.

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Predictions of xenobiotic hepatic clearance in humans using in vitro-to-in vivo extrapolation methods are frequently inaccurate and problematic. Multiple strategies are being pursued to disentangle responsible mechanisms. The objective of this work is to evaluate the feasibility of using insights gained from independent virtual experiments on two model systems to begin unraveling responsible mechanisms. The virtual culture is a software analog of hepatocytes in vitro, and the virtual human maps to hepatocytes within a liver within an idealized model human. Mobile objects (virtual compounds) ma

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Yin, Wencui, Reem I. Alwabli, Mohamed W. Attwa, A. F. M. Motiur Rahman, and Adnan A. Kadi. "Simvastatin: In Vitro Metabolic Profiling of a Potent Competitive HMG-CoA Reductase Inhibitor." Separations 9, no. 12 (2022): 400. http://dx.doi.org/10.3390/separations9120400.

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Simvastatin (SV) is a semisynthetic derivative of lovastatin (LV), which is biosynthetically produced from the fungus Aspergillus terreus and has a high log p value (log p = 4.39)and thus high hepatic extraction and high efficacy in controlling cholesterol synthesis. The current study was undertaken to investigate the metabolic profile of SV using various mass spectrometry (MS) platforms. Metabolic profiling was studied in in vitro models, rat liver microsomes (RLMs), and isolated perfused rat liver hepatocytes (RLHs) using both ion trap and triple quadruple LC–MS/MS systems. A total of 29 met

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Lehwald, Nadja, Constanze Duhme, Iryna Pinchuk, et al. "Platelets Boost Recruitment of CD133+ Bone Marrow Stem Cells to Endothelium and the Rodent Liver—The Role of P-Selectin/PSGL-1 Interactions." International Journal of Molecular Sciences 21, no. 17 (2020): 6431. http://dx.doi.org/10.3390/ijms21176431.

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We previously demonstrated that clinical administration of mobilized CD133+ bone marrow stem cells (BMSC) accelerates hepatic regeneration. Here, we investigated the potential of platelets to modulate CD133+BMSC homing to hepatic endothelial cells and sequestration to warm ischemic livers. Modulatory effects of platelets on the adhesion of CD133+BMSC to human and mouse liver-sinusoidal- and micro- endothelial cells (EC) respectively were evaluated in in vitro co-culture systems. CD133+BMSC adhesion to all types of EC were increased in the presence of platelets under shear stress. This platelet

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Mitani, T., T. Nagai, T. Masutani, et al. "227 DIFFERENTIATION OF HEPATOCYTE-LIKE CELLS FROM MOUSE EMBRYONIC STEM CELLS IN A MONOLAYER CULTURE SYSTEM." Reproduction, Fertility and Development 19, no. 1 (2007): 230. http://dx.doi.org/10.1071/rdv19n1ab227.

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Embryonic stem (ES) cells can be differentiated in vitro into a variety of cell lineages. In vitro differentiation of ES cells, therefore, provides a model system for organogenesis as well as an innovative approach for regenerative medicine. However, current in vitro hepatic differentiation systems from ES cells require embryoid body formation, and such systems achieve quite low differentiation efficacy. In this study, in order to examine a system for preparation of significant numbers of hepatocytes from ES cells, mouse ES cells were directly differentiated into hepatocyte-like cells using mo

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Kermanizadeh, Ali, and Wolfgang Moritz. "Next generation in vitro primary hepatic cell test systems—their suitability as an alternative to in vivo testing?" Hepatobiliary Surgery and Nutrition 9, no. 1 (2020): 103–5. http://dx.doi.org/10.21037/hbsn.2019.09.09.

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Morcillo, Yolanda, Gemma Janer, Sean C. M. O'Hara, David R. Livingstone, and Cinta Porte. "INTERACTION OF TRIBUTYLTIN WITH HEPATIC CYTOCHROME P450 AND URIDINE DIPHOSPHATE–GLUCURONOSYL TRANSFERASE SYSTEMS OF FISH: IN VITRO STUDIES." Environmental Toxicology and Chemistry 23, no. 4 (2004): 990. http://dx.doi.org/10.1897/034-262.

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Mun, Seon Ju, Jaeseo Lee, Yongbo Shin, and Myung Jin Son. "Advanced human liver models for the assessment of drug-induced liver injury." Organoid 2 (July 25, 2022): e17. http://dx.doi.org/10.51335/organoid.2022.2.e17.

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Drug safety issues continue to occur even with drugs that are approved after the completion of clinical studies. Drug-induced liver injury (DILI) is a major obstacle to drug development, because the liver is the primary site of drug metabolism, and injuries caused during this process are severe. Conventional in vitro human liver models, such as 2-dimensional hepatic cell lines, lack in vivo physiological relevance, and animal studies have limitations in the form of species differences and regulatory restrictions. To resolve this issue, an increasing number of 3-dimensional human liver systems,

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Williams, Dominic P. "Application of hepatocyte-like cells to enhance hepatic safety risk assessment in drug discovery." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1750 (2018): 20170228. http://dx.doi.org/10.1098/rstb.2017.0228.

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Hepatic stress and injury from drugs continues to be a major concern within the pharmaceutical industry, leading to preclinical and clinical attrition precautionary warnings and post-market withdrawal of drugs. There is a requirement for more predictive and mechanistically accurate models to aid risk assessment. Primary human hepatocytes, subject to isolation stress, cryopreservation, donor-to-donor variation and a relatively short period of functional capability in two-dimensional cultures, are not suitable for high-throughput screening procedures. There are two areas within the drug discover

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Rizzardini, M., M. Carelli, M. R. Cabello Porras, and L. Cantoni. "Mechanisms of endotoxin-induced haem oxygenase mRNA accumulation in mouse liver: synergism by glutathione depletion and protection by N-acetylcysteine." Biochemical Journal 304, no. 2 (1994): 477–83. http://dx.doi.org/10.1042/bj3040477.

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In in vitro systems haem oxygenase-1 (HO-1) mRNA increases after exposure to agents causing oxidative stress. We lowered cellular antioxidant defence systems in vivo by giving mice increasing doses (0.15 g/kg-1.6 g/kg) of DL-buthionine-(S,R)-sulphoximine (BSO), a specific inhibitor of glutathione synthesis. Maximum glutathione depletion (80%) coincided with maximum hepatic HO-1 mRNA accumulation (about 20 times), whereas with 50% depletion, accumulation was only doubled. It has been suggested that reactive oxygen and nitrogen intermediates are involved in hepatic toxicity of endotoxin (lipopol

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Leedale, Joseph A., Jonathan A. Kyffin, Amy L. Harding, et al. "Multiscale modelling of drug transport and metabolism in liver spheroids." Interface Focus 10, no. 2 (2020): 20190041. http://dx.doi.org/10.1098/rsfs.2019.0041.

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In early preclinical drug development, potential candidates are tested in the laboratory using isolated cells. These in vitro experiments traditionally involve cells cultured in a two-dimensional monolayer environment. However, cells cultured in three-dimensional spheroid systems have been shown to more closely resemble the functionality and morphology of cells in vivo . While the increasing usage of hepatic spheroid cultures allows for more relevant experimentation in a more realistic biological environment, the underlying physical processes of drug transport, uptake and metabolism contributi

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Zanieri, Francesca, Ana Levi, David Montefusco, et al. "Exogenous Liposomal Ceramide-C6 Ameliorates Lipidomic Profile, Energy Homeostasis, and Anti-Oxidant Systems in NASH." Cells 9, no. 5 (2020): 1237. http://dx.doi.org/10.3390/cells9051237.

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In non-alcoholic steatohepatitis (NASH), many lines of investigation have reported a dysregulation in lipid homeostasis, leading to intrahepatic lipid accumulation. Recently, the role of dysfunctional sphingolipid metabolism has also been proposed. Human and animal models of NASH have been associated with elevated levels of long chain ceramides and pro-apoptotic sphingolipid metabolites, implicated in regulating fatty acid oxidation and inflammation. Importantly, inhibition of de novo ceramide biosynthesis or knock-down of ceramide synthases reverse some of the pathology of NASH. In contrast,

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Das, Sonjit, Swarnalata Joardar, Prasenjit Manna, et al. "Carnosic Acid, a Natural Diterpene, Attenuates Arsenic-Induced Hepatotoxicity via Reducing Oxidative Stress, MAPK Activation, and Apoptotic Cell Death Pathway." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–24. http://dx.doi.org/10.1155/2018/1421438.

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The present studies have been executed to explore the protective mechanism of carnosic acid (CA) against NaAsO2-induced hepatic injury. CA exhibited a concentration dependent (1–4 μM) increase in cell viability against NaAsO2 (12 μM) in murine hepatocytes. NaAsO2 treatment significantly enhanced the ROS-mediated oxidative stress in the hepatic cells both in in vitro and in vivo systems. Significant activation of MAPK, NF-κB, p53, and intrinsic and extrinsic apoptotic signaling was observed in NaAsO2-exposed hepatic cells. CA could significantly counteract with redox stress and ROS-mediated sig

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Okaya, Tomohisa, та Alex B. Lentsch. "Peroxisome proliferator-activated receptor-α regulates postischemic liver injury". American Journal of Physiology-Gastrointestinal and Liver Physiology 286, № 4 (2004): G606—G612. http://dx.doi.org/10.1152/ajpgi.00191.2003.

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Peroxisome proliferator-activated receptor-α (PPARα) is a transcription factor that in some in vitro systems has been linked with downregulation of proinflammatory mediators, thus implicating a potential role for PPARα in the regulation of inflammatory processes. Hepatic ischemia-reperfusion injury is characterized by an intense acute inflammatory response that is dependent on a number of proinflammatory mediators. PPARα is abundantly expressed in hepatic parenchymal cells but not in Kupffer cells. This study examined whether PPARα is involved in regulation of the hepatic inflammatory response

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Hughes, David J., Tomasz Kostrzewski, and Emma L. Sceats. "Opportunities and challenges in the wider adoption of liver and interconnected microphysiological systems." Experimental Biology and Medicine 242, no. 16 (2017): 1593–604. http://dx.doi.org/10.1177/1535370217708976.

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Liver disease represents a growing global health burden. The development of in vitro liver models which allow the study of disease and the prediction of metabolism and drug-induced liver injury in humans remains a challenge. The maintenance of functional primary hepatocytes cultures, the parenchymal cell of the liver, has historically been difficult with dedifferentiation and the consequent loss of hepatic function limiting utility. The desire for longer term functional liver cultures sparked the development of numerous systems, including collagen sandwiches, spheroids, micropatterned co-cultu

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Liu, Tianxiong, Yujiao Li, Xianzhe Chen, Xiaoming Zhao, Jianfang Wang, and Dongyi Zhang. "Fabrication of pH-sensitive graphene oxide–Benazepril carrier as biosafety controlled release systems." Journal of Applied Biomaterials & Functional Materials 18 (January 2020): 228080002096347. http://dx.doi.org/10.1177/2280800020963471.

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A novel graphene oxide (GO)-based carrier was fabricated for the controlled release of Benazepril (BENA). Freeze dried samples of GO–BENA carrier were prepared for controlled drug release at different pHs (pH = 2, 7, and 10) and release kinetics indicate BENA desorption from GO is by Fickian diffusion. The BENA yield from the carrier amounted to ~55% of the adsorbed material in a strongly acidic medium after 50 h. Binding fractions of BENA to 10 mg/L GO was determined for different solution concentrations of the drug. In vitro assays of cell proliferation (WST-1 kit), cell structural integrity

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Lidström-Olsson, B., and K. Wikvall. "The role of sterol carrier protein2 and other hepatic lipid-binding proteins in bile-acid biosynthesis." Biochemical Journal 238, no. 3 (1986): 879–84. http://dx.doi.org/10.1042/bj2380879.

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The ability of different lipid-binding proteins in liver cytosol to affect enzyme activities in bile-acid biosynthesis was studied in whole microsomes (microsomal fractions) and mitochondria and in purified enzyme systems. Sterol carrier protein2 stimulated the 7 alpha-hydroxylation of cholesterol and the 12 alpha-hydroxylation of 5 beta-cholestane-3 alpha, 7 alpha-diol in microsomes and the 26-hydroxylation of cholesterol in mitochondria 2-3-fold. It also stimulated the oxidation of 5-cholestene-3 beta, 7 alpha-diol into 7 alpha-hydroxy-4-cholesten-3-one in microsomes. The stimulatory effect

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