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Journal articles on the topic 'Alcohol Rats'

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Published: 4 June 2021

Last updated: 18 February 2022

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1

GHELARDINI, C., N. GALEOTTI, V. MARCHESE, and BARTOLINIA. "SARDINIAN ALCOHOL PREFERRING RATS." Behavioural Pharmacology 7, Supplement 1 (May 1996): 43. http://dx.doi.org/10.1097/00008877-199605001-00098.

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2

Bon, L. I., and S. M. Zimatkin. "DISTURBANCES IN BRAIN CORTEX NEURONS FOLLOWING PRENATAL ALCOHOL EXPOSURE IN RATS." Journal of the Grodno State Medical University 16, no. 1 (2018): 23–27. http://dx.doi.org/10.25298/2221-8785-2018-16-1-23-27.

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3

Gilpin, N. W., H. N. Richardson, L. Lumeng, and G. F. Koob. "Dependence-Induced Alcohol Drinking by Alcohol-Preferring (P) Rats and Outbred Wistar Rats." Alcoholism: Clinical and Experimental Research 32, no. 9 (September 2008): 1688–96. http://dx.doi.org/10.1111/j.1530-0277.2008.00678.x.

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4

Ham, Ju Ri, Ra-Yeong Choi, Hae-In Lee, and Mi-Kyung Lee. "Protective Effects of Methoxsalen Supplementation on Chronic Alcohol-induced Osteopenia and Steatosis in Rats." Molecules 25, no. 5 (March 5, 2020): 1177. http://dx.doi.org/10.3390/molecules25051177.

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Osteopenia or osteoporosis occurs frequently in alcoholics and patients with alcoholic fatty liver disease. Methoxsalen (MTS), 8-methoxypsoralen, improved osteoporosis in ovariectomized and diabetic mouse models; however, its effects on alcohol-induced osteopenia and steatosis have not been reported. This study examined the effects of MTS on alcohol-induced bone loss and steatosis. Rats in the alcohol groups were fed a Liber-DeCarli liquid diet containing 36% of its calories as alcohol. MTS was at 0.005% in their diet, while alendronate (positive control; 500 μg/kg BW/day) was administered orally for eight weeks. The pair-fed group received the same volume of isocaloric liquid diet containing dextrin-maltose instead of alcohol as the alcohol control group consumed the previous day. In the alcohol-fed rats, the MTS and alendronate increased the bone volume density, bone surface density and trabecular number, while the bone specific surface, trabecular separation and structure model index were decreased in the tibia. MTS down-regulated tibial tartrate-resistant acid phosphatase 5 (TRAP) expression compared to the alcohol control group. MTS or alendronate prevented chronic alcohol-induced hepatic lipid accumulation and the triglyceride level in the alcohol-fed rats by decreasing the lipogenic enzyme activities and increasing the fatty acid oxidation enzyme activities. MTS reduced significantly the serum levels of alcohol, TRAP and tumor necrosis factor-α compared to the alcohol control group. Overall, these results suggest that MTS is likely to be an alternative agent for alcoholic osteopenia and hepatosteatosis.

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5

IORDANSKAYA, T. E., N. A. KRUPINA, I. N. ORLOVA, and N. B. PANKOVA. "INCREASE IN ALCOHOL CONSUMPTION WITH ALCOHOL EXPERIENCE IN RATS." Behavioural Pharmacology 7, Supplement 1 (May 1996): 52. http://dx.doi.org/10.1097/00008877-199605001-00118.

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6

Ehlers, Cindy L., Brendan M. Walker, Jerry P. Pian, Jennifer L. Roth, and Craig J. Slawecki. "Increased alcohol drinking in isolate-housed alcohol-preferring rats." Behavioral Neuroscience 121, no. 1 (2007): 111–19. http://dx.doi.org/10.1037/0735-7044.121.1.111.

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7

Myers, R. D., and Miles F. Lankford. "Suppression of Alcohol Preference in High Alcohol Drinking Rats." Neuropsychopharmacology 14, no. 2 (February 1996): 139–49. http://dx.doi.org/10.1016/0893-133x(95)00081-n.

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8

Loi, Barbara, Giancarlo Colombo, Paola Maccioni, Mauro A. M. Carai, Flavia Franconi, and Gian Luigi Gessa. "High alcohol intake in female Sardinian alcohol-preferring rats." Alcohol 48, no. 4 (June 2014): 345–51. http://dx.doi.org/10.1016/j.alcohol.2014.01.001.

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9

Rezvani, Amir H., and David S. Janowsky. "Decreased alcohol consumption by verapamil in alcohol preferring rats." Progress in Neuro-Psychopharmacology and Biological Psychiatry 14, no. 4 (January 1990): 623–31. http://dx.doi.org/10.1016/0278-5846(90)90013-7.

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10

Nwaogu, I. C. "Foetal Alcohol Syndrome: Growth Rate of Bones in Rats." Journal of Applied Animal Research 22, no. 2 (December 2002): 249–53. http://dx.doi.org/10.1080/09712119.2002.9706406.

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11

Lang, Charles H., Robert A. Frost, and Thomas C. Vary. "Skeletal muscle protein synthesis and degradation exhibit sexual dimorphism after chronic alcohol consumption but not acute intoxication." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1497—E1506. http://dx.doi.org/10.1152/ajpendo.00603.2006.

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Epidemiological evidence suggests alcoholic myopathy is more severe in females than males, but comparable animal studies are lacking that make elucidating the biochemical locus for this defect problematic. The present study determined whether skeletal muscle protein synthesis and markers of degradation exhibit a sexual dimorphic response to either chronic alcohol consumption or acute intoxication. Male and female rats were fed an alcohol-containing diet, pair-fed for 26 wk (chronic), or received an intraperitoneal injection of alcohol (acute). In males, chronic alcohol decreased gastrocnemius protein synthesis by 20%. This reduction was associated with a twofold increase in the inactive eukaryotic initiation factor (eIF) 4E·4E-binding protein 1 (4E-BP1) complex and a 60% reduction in the active eIF4E·eIF4G complex. This redistribution of eIF4E was associated with decreased phosphorylation of both 4E-BP1 and eIF4G (50–55%). The phosphorylation of ribosomal protein S6 was also reduced 60% in alcohol-consuming male rats. In contrast, neither rates of protein synthesis nor indexes of translation initiation in muscle were altered in alcohol-fed female rats despite blood alcohol levels comparable to males. Chronic alcohol ingestion did not alter atrogin-1 or muscle RING finger-1 mRNA content (biomarkers of muscle proteolysis) in males but increased their expression in females 50–100%. Acute alcohol intoxication produced a comparable decrease in muscle protein synthesis and translation initiation in both male and female rats. Our data demonstrate a sexual dimorphism for muscle protein synthesis, translation initiation, and proteolysis in response to chronic, but not acute, alcohol intoxication; however, they do not support evidence indicating females are more sensitive toward the development of alcoholic skeletal muscle myopathy.

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12

Miyamae, Masami, S. Albert Camacho, Hui-Zhong Zhou, Ivan Diamond, and Vincent M. Figueredo. "Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 1 (July 1, 1998): H50—H56. http://dx.doi.org/10.1152/ajpheart.1998.275.1.h50.

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We recently discovered that regular alcohol consumption reduces ischemia-reperfusion injury to the same degree as ischemic preconditioning in guinea pig hearts. Ischemic preconditioning, like this cardioprotective effect of alcohol, is mediated by adenosine signaling in guinea pigs. In rats, ischemic preconditioning may be mediated predominantly by α1-adrenergic signaling. To be certain that this protective effect of alcohol is a general biological response, we searched for alcohol’s cardioprotection in rat and identified a potential signaling mechanism. Hearts isolated from alcohol-fed guinea pigs and rats were subjected to ischemia-reperfusion. Hearts from alcohol-fed animals showed greater recovery of left ventricular developed pressure than controls (guinea pigs, 46 vs. 29%; rats, 50 vs. 31%) and decreased myocyte necrosis assessed by creatine kinase release (guinea pigs, 204 ± 42 vs. 440 ± 70 U ⋅ ml−1 ⋅ g dry wt−1; rats 158 ± 13 vs. 328 ± 31 U ⋅ ml−1 ⋅ g dry wt−1). Adenosine receptor blockade [8-( p-sulfophenyl)theophylline] abolished alcohol’s protection in guinea pig but not rat hearts. By contrast, α1-adrenergic blockade (prazosin) abolished alcohol’s protection in rat but not guinea pig hearts. We conclude that regular alcohol consumption reduces ischemia-reperfusion injury and is mediated by species-specific signaling mechanisms. A major goal of cardiovascular research is to find a pharmacologically induced chronic state of preconditioning. Understanding the mechanisms of alcohol’s cardioprotection against ischemia-reperfusion injury may aid in reaching this goal.

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13

Smith, D. G., J. E. Learn, W. J. McBride, L. Lumeng, T. K. Li, and J. M. Murphy. "Alcohol-Naive Alcohol-Preferring (P) Rats Exhibit Higher Local Cerebral Glucose Utilization Than Alcohol-Nonpreferring (NP) and Wistar Rats." Alcoholism: Clinical and Experimental Research 25, no. 9 (September 2001): 1309–16. http://dx.doi.org/10.1111/j.1530-0277.2001.tb02352.x.

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14

Learn, Jennifer E., Daniel G. Smith, William J. McBride, Lawrence Lumeng, and Ting-Kai Li. "Local Cerebral Glucose Utilization Rates in Alcohol-Naive High-Alcohol-Drinking (HAD) and Low-Alcohol-Drinking (LAD) Rats." Alcoholism: Clinical and Experimental Research 25, no. 4 (April 2001): 517–23. http://dx.doi.org/10.1111/j.1530-0277.2001.tb02245.x.

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15

Kołota, Aleksandra, Dominika Głąbska, Michał Oczkowski, and Joanna Gromadzka-Ostrowska. "Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages." Nutrients 12, no. 1 (January 6, 2020): 158. http://dx.doi.org/10.3390/nu12010158.

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Typical alcohol consumption begins in the adolescence period, increasing the risk of alcoholic liver disease (ALD) in adolescents and young adults, and while the pathophysiology of ALD is still not completely understood, it is believed that oxidative stress may be the major contributor that initiates and promotes the progression of liver damage. The aim of the present study was to assess the influence of alcohol consumption on the markers of oxidative stress and liver inflammation in the animal model of prolonged alcohol consumption in adolescents using various alcoholic beverages. In a homogenic group of 24 male Wistar rats (4 groups—6 animals per group), since 30th day of life, in order to mimic the alcohol consumption since adolescence, animals received (1) no alcoholic beverage (control group), (2) ethanol solution, (3) red wine, or (4) beer (experimental groups) for 6 weeks. Afterwards, the activities of alcohol dehydrogenase (ADH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of cytochrome P450-2E1 (CYP2E1), thiobarbituric acid-reactive substances (TBARS), protein carbonyl groups, tumor necrosis factor-α (TNF-α), and interleukine-10 (IL-10) were measured in liver homogenates. The difference between studied groups was observed for CYP2E1 and protein carbonyl groups levels (increased levels for animals receiving beer compared with control group), as well as for ALT activity (decreased activity for animals receiving beer compared with other experimental groups) (p < 0.05). The results suggested that some components of beer, other than ethanol, are responsible for its influence on the markers of oxidative stress and liver inflammation observed in the animal model of prolonged alcohol consumption in adolescents. Taking this into account, beer consumption in adolescents, which is a serious public health issue, should be assessed in further studies to broaden the knowledge of the progression of liver damage caused by alcohol consumption in this group.

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16

Tattoli, M. "Neurofunctional Effects of Developmental Alcohol Exposure in Alcohol-Preferring and Alcohol-Nonpreferring Rats." Neuropsychopharmacology 24, no. 6 (June 2001): 691–705. http://dx.doi.org/10.1016/s0893-133x(00)00225-6.

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17

Akala, Emmanuel O., Hu Wang, and Adedayo Adedoyin. "Disposition of Naltrexone after Intravenous Bolus Administration in Wistar Rats, Low-Alcohol-Drinking Rats and High-Alcohol-Drinking Rats." Neuropsychobiology 58, no. 2 (2008): 81–90. http://dx.doi.org/10.1159/000159776.

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18

Ingman, Kimmo, Aapo Honkanen, Petri Hyytiä, Matti O. Huttunen, and Esa R. Korpi. "Risperidone reduces limited access alcohol drinking in alcohol-preferring rats." European Journal of Pharmacology 468, no. 2 (May 2003): 121–27. http://dx.doi.org/10.1016/s0014-2999(03)01669-8.

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19

COLOMBO, G., R. AGABIO, C. LOBINA, R. REALI, F. FADDA, and G. L. GESSA. "CHARACTERIZATION OF ALCOHOL DRINKING BEHAVIOUR IN SARDINIAN ALCOHOL-PREFERRING RATS." Behavioural Pharmacology 7, Supplement 1 (May 1996): 19. http://dx.doi.org/10.1097/00008877-199605001-00041.

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20

Maccioni, Paola, Salvatore Serra, Giovanni Vacca, Alessandro Orrù, Daniela Pes, Roberta Agabio, Giovanni Addolorato, Mauro A. M. Carai, Gian Luigi Gessa, and Giancarlo Colombo. "Baclofen-induced reduction of alcohol reinforcement in alcohol-preferring rats." Alcohol 36, no. 3 (July 2005): 161–68. http://dx.doi.org/10.1016/j.alcohol.2005.08.003.

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21

Stewart, R. B., J. M. Murphy, W. J. McBride, L. Lumeng, and T. K. Li. "Place conditioning with alcohol in alcohol-preferring and -nonpreferring rats." Pharmacology Biochemistry and Behavior 53, no. 3 (March 1996): 487–91. http://dx.doi.org/10.1016/0091-3057(95)02102-7.

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22

Ciccocioppo, Roberto, Izabela Panocka, Carlo Polidori, Domenico Regoli, and M. Massi. "Effect of nociceptin on alcohol intake in alcohol-preferring rats." Psychopharmacology 141, no. 2 (January 11, 1999): 220–24. http://dx.doi.org/10.1007/s002130050828.

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23

Thomas, Jennifer D., Teresa L. Burchette, Hector D. Dominguez, and Edward P. Riley. "Neonatal alcohol exposure produces more severe motor coordination deficits in high alcohol sensitive rats compared to low alcohol sensitive rats." Alcohol 20, no. 1 (January 2000): 93–99. http://dx.doi.org/10.1016/s0741-8329(99)00080-4.

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24

Smith, D. G., J. E. Learn, W. J. McBride, L. Lumeng, T. K. Li, and J. M. Murphy. "Alcohol-Na??ve Alcohol-Preferring (P) Rats Exhibit Higher Local Cerebral Glucose Utilization Than Alcohol-Nonpreferring (NP) and Wistar Rats." Alcoholism: Clinical and Experimental Research 25, no. 9 (September 2001): 1309–16. http://dx.doi.org/10.1097/00000374-200109000-00010.

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25

Kodidela, Swarnalatha, Suresh Govatati, Sumanth Kumar Matha, Swapna Vahini Korla, B. Prathap Naidu, Lokesh Thippannagari, Pallaval Veera Bramhachari, Manjula Bhanoori, and Varadacharyulu Nallanchakravarthula. "Impact of alcohol on hepatic mitochondrial DNA damage in streptozotocin diabetic rats." Journal of Experimental and Applied Animal Sciences 2, no. 2 (February 6, 2017): 90. http://dx.doi.org/10.20454/jeaas.2017.1225.

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Mitochondrial dysfunction with increased production of reactive oxygen species (ROS) is a characteristic feature of diabetes which is associated with damage of mitochondrial DNA (mtDNA). Alcohol metabolism generates ROS with enhanced oxidative stress leading to damage of cellular constituents including mtDNA. The aim of the present study is to investigate the impact of alcohol consumption on hepatic mtDNA damage in diabetic rats. MtDNA was isolated from hepatic tissues of non-diabetic and streptozotocin induced diabetic rats after alcohol treatment. Comprehensive screening of mtDNA displacement loop (D-loop) was carried out by PCR-Sanger’s sequencing analysis. MtDNA deletions were analyzed by long-extension PCR. Furthermore, activities of enzymatic and non-enzymatic antioxidants were measured in hepatic tissue of all rats. Our results showed increased frequency of D-loop mutations in alcoholic-diabetic rats when compared to diabetic or alcoholic non-diabetic rats. DNA mfold analysis predicted higher free energy for 15507C, 15560T and 16116C alleles compared to their corresponding wild alleles which represents less stable secondary structures with negative impact on overall mtDNA function. MtDNA deletions were observed in all experimental groups except controls. Markedly decreased activities of antioxidant enzymes viz., GPx, SOD, catalase and GSH content was identified in alcoholic-diabetic rats when compared to remaining groups. In conclusion, decreased GSH content and lowered activity of catalase, SOD and GPx favor the environment for oxidative stress, which might lead to exacerbation of hepatic mitochondrial DNA damage in diabetic rats receiving alcohol.

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26

Plapp, Bryce V., Kevin G. Leidal, Bruce P. Murch, and David W. Green. "Contribution of liver alcohol dehydrogenase to metabolism of alcohols in rats." Chemico-Biological Interactions 234 (June 2015): 85–95. http://dx.doi.org/10.1016/j.cbi.2014.12.040.

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27

Learn, Jennifer E., Daniel G. Smith, William J. McBride, Lawrence Lumeng, and Ting-Kai Li. "Local Cerebral Glucose Utilization Rates in Alcohol-Na??ve High???Alcohol-Drinking (HAD) and Low???Alcohol-Drinking (LAD) Rats." Alcoholism: Clinical and Experimental Research 25, no. 4 (April 2001): 517–23. http://dx.doi.org/10.1097/00000374-200104000-00007.

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28

Choi, Ra-Yeong, Ju Ri Ham, Hyo-Seon Ryu, Sang Suk Lee, Michelle A. Miguel, Man-Jeong Paik, Moongi Ji, et al. "Defatted Tenebrio molitor Larva Fermentation Extract Modifies Steatosis, Inflammation and Intestinal Microflora in Chronic Alcohol-Fed Rats." Nutrients 12, no. 5 (May 14, 2020): 1426. http://dx.doi.org/10.3390/nu12051426.

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This study examined the effects of defatted mealworm fermentation extract (MWF) on alcoholic liver injury in rats. The rats were fed either a Lieber-DeCarli control (Con) or alcohol liquid diet (EtOH). The alcohol-fed rats were administered MWF (50, 100, or 200 mg/kg/day) and silymarin (200 mg/kg/day) orally for eight weeks. MWF prevented alcohol-induced hepatocellular damage by decreasing their serum aspartate transaminase, alanine transaminase, and gamma-glutamyl transpeptidase levels significantly compared to the EtOH group. MWF effectively reduced the relative hepatic weight, lipid contents, and fat deposition, along with the down-regulation of transcriptional factors and genes involved in lipogenesis compared to the EtOH group. It also enhanced the antioxidant defense system by elevating the glutathione level and glutathione reductase activity. MWF attenuated the alcohol-induced inflammatory response by down-regulating hepatic inflammation-associated proteins expression, such as phosphorylated-inhibitor of nuclear factor-kappa B-alpha and tumor necrosis factor-alpha, in chronic alcohol-fed rats. Furthermore, sequencing analysis in the colonic microbiota showed that MWF tended to increase Lactobacillus johnsonii reduced by chronic alcohol consumption. These findings suggest that MWF can attenuate alcoholic liver injury by regulating the lipogenic and inflammatory pathway and antioxidant defense system, as well as by partially altering the microbial composition.

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29

KUCHERYANU, V. G., G. N. KRYZHANOVSKY, E. B. KLADKEVICH, and N. A. KRUPINA. "NEUROCHEMISTRY OF ALCOHOL-PREFERRING AA RATS." Behavioural Pharmacology 7, Supplement 1 (May 1996): 59. http://dx.doi.org/10.1097/00008877-199605001-00134.

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30

Kiefer, Stephen W., and Joel M. Dopp. "Taste reactivity to alcohol in rats." Behavioral Neuroscience 103, no. 6 (1989): 1318–26. http://dx.doi.org/10.1037/0735-7044.103.6.1318.

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31

Heyman, G. M., Keith Gendel, and Jason Goodman. "Inelastic demand for alcohol in rats." Psychopharmacology 144, no. 3 (June 21, 1999): 213–19. http://dx.doi.org/10.1007/s002130050996.

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32

Rowland, Neil E., and Michael Barnett. "Sham ingestion of alcohol in rats." Alcohol 9, no. 1 (January 1992): 75–77. http://dx.doi.org/10.1016/0741-8329(92)90013-z.

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33

Kumar Chandra, Hemeshwer, Gita Mishra, Nisha Sahu, Satendra Kumar Nirala, and Monika Bhadauria. "EFFECT OF RUTIN AGAINST HIGH-FAT DIET AND ALCOHOL-INDUCED ALTERATIONS IN HEMATOLOGICAL VARIABLES OF RATS." Asian Journal of Pharmaceutical and Clinical Research 11, no. 11 (November 7, 2018): 186. http://dx.doi.org/10.22159/ajpcr.2018.v11i11.27588.

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Objectives: Alcohol abuse leads to several diseases and millions of death worldwide. High-fat diet (HFD) is major contributor of non-alcoholic liver diseases and obesity. Combined consumption of HFD and alcohol has deleterious effect on blood cells. This study was carried out to evaluate the protective effect of rutin against combined consumption of HFD and alcohol-induced hematological alterations.Methods: HFD 30% and ethanol 10% were administered for 4 weeks for induction of toxicity. Rutin (10, 20, and 40 mg/kg) and 50 mg/kg dose of silymarin were administered along with HFD and alcohol for 4 weeks.Results: Combined consumption of HFD and alcohol increased mean corpuscular volume, total leukocytes count, eosinophil and monocyte, and decreased hematocrit and platelets. Administration of rutin improved hematological variables altered by HFD and alcohol consumption.Conclusion: The present study concluded that administration of rutin may alleviate HFD and alcohol-induced hematological alterations by scavenging free radicals generation.

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34

Li, Zhaoping, Zhenzhen Hu, Yan Meng, Hongzhao Xu, Yali Wei, Deqiang Shen, Hao Bai, Huacai Yuan, and Liyong Chen. "miR-155-5p upregulation ameliorates myocardial insulin resistance via mTOR signaling in chronic alcohol drinking rats." PeerJ 9 (April 5, 2021): e10920. http://dx.doi.org/10.7717/peerj.10920.

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Background Chronic alcohol intake is associated with an increased risk of alcoholic cardiomyopathy, which may present with pathological changes such as myocardial insulin resistance, leading to ventricular dilation and cardiac dysfunction. Although a correlation between microRNA-155 (miR-155) and insulin signaling has been identified, the underlying mechanism has not been elucidated to date. The purpose of the study was to determine whether overexpression of miR-155-5p in vivo could ameliorate chronic alcohol-induced myocardial insulin resistance and cardiac dysfunction. Material and Methods Wistar rats were fed with either alcohol or water for 20 weeks to establish chronic alcohol intakes model. Then the alcohol group were divided into three groups: model group, miRNA-155 group and AAV-NC group. Rats undergoing alcohol treatment were injected with AAV-miRNA-155 (adeno-associated virus 9) or its negative control AAV-NC, respectively. Gene expression was determined by real-time PCR, and protein expression was determined by western blot. Echocardiography was performed to assess terminal cardiac function. Insulin responsiveness was determined through the quantification of phosphorylated insulin receptor substrate 1 (ser 307) and phosphorylated insulin receptor (Tyr 1185) levels. Results We found that cardiac function was attenuated in chronic alcohol intake rats, with an activated mammalian target of rapamycin (mTOR) signaling pathway, accompanied by an increase in p-IRS1(ser 307) and a decrease in p-IR (Tyr 1185) level in myocardial tissue. Also, alcohol drinking significantly up-regulated miR-155-5p level and its overexpression decreased p-IRS1 (ser 307) and increased p-IR (Tyr 1185) levels, and meanwhile inhibited the mTOR signaling pathway. Conclusion miR-155-5p upregulation ameliorates myocardial insulin resistance via the mTOR signaling in chronic alcohol drinking rats. We propose that miR-155 may serve as a novel potential therapeutic target for alcoholic heart disease.

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35

Phunchago, Nattaporn, Jintanaporn Wattanathorn, and Kowit Chaisiwamongkol. "Tiliacora triandra, an Anti-Intoxication Plant, Improves Memory Impairment, Neurodegeneration, Cholinergic Function, and Oxidative Stress in Hippocampus of Ethanol Dependence Rats." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/918426.

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Oxidative stress plays an important role in brain dysfunctions induced by alcohol. Since less therapeutic agent against cognitive deficit and brain damage induced by chronic alcohol consumption is less available, we aimed to assess the effect ofTiliacora triandraextract, a plant possessing antioxidant activity, on memory impairment, neuron density, cholinergic function, and oxidative stress in hippocampus of alcoholic rats. Male Wistar rats were induced ethanol dependence condition by semivoluntary intake of alcohol for 15 weeks. Alcoholic rats were orally givenT. triandraat doses of 100, 200, and 400 mg·kg−1BW for 14 days. Memory assessment was performed every 7 days while neuron density, activities of AChE, SOD, CAT, and GSH-Px and, MDA level in hippocampus were assessed at the end of study. Interestingly, the extract mitigated the increased escape latency, AChE and MDA level. The extract also mitigated the decreased retention time, SOD, CAT, and GSH-Px activities, and neurons density in hippocampus induced by alcohol. These data suggested that the extract improved memory deficit in alcoholic rats partly via the decreased oxidative stress and the suppression of AChE. Therefore,T. triandrais the potential reagent for treating brain dysfunction induced by alcohol. However, further researches are necessary to understand the detail mechanism and possible active ingredient.

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36

Li, Jun, Barbara A. French, Paul Fu, Fawzia Bardag-Gorce, and Samuel W. French. "Mechanism of the alcohol cyclic pattern: role of catecholamines." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 2 (August 2003): G442—G448. http://dx.doi.org/10.1152/ajpgi.00093.2003.

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The cause of the urinary alcohol level (UAL) cycle in rats fed ethanol at a constant rate has been shown to involve the hypothalamic-pituitary thyroid axis. Because the effect of thyroid hormone on the metabolic rate is augmented by catecholamines, the role of catecholamines was investigated by using the intragastric ethanol feeding model of alcoholic liver disease in which the UAL cycles over a 6- to 10-day period. The diet was supplemented with ephedrine and caffeine to test the hypothesis that the UAL cycle involves catecholamines. The UAL was followed to see whether the cycle was ablated by catecholamine supplements. Ethanol fed alone increased the blood levels of catecholamines significantly more than did ephedrine fed alone. However, blood catecholamine levels were significantly higher when ethanol was fed with ephedrine compared with the sum of ethanol and ephedrine fed alone. This indicated that the effect of ethanol and ephedrine were synergistic. The UAL cycle was completely ablated in the ethanol + ephedrine-fed rats. These rats tolerated a much higher dose of ethanol, indicating that they metabolized alcohol faster due to an increase in metabolic rate caused by ephedrine. In the ethanol + ephedrine-fed rats the liver pathology included significantly higher alanine amino transferase (ALT) in the blood and centrilobular ischemic necrosis in the liver. Necrosis was not present in the rats fed ephedrine alone. In conclusion, catecholamine supplements prevented the UAL cycle by increasing the metabolic rate to the point at which fluctuations in the metabolic rate caused by alcohol were prevented.

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37

Krahn, Dean D., and Blake A. Gosnell. "Fat-preferring rats consume more alcohol than carbohydrate-preferring rats." Alcohol 8, no. 4 (July 1991): 313–16. http://dx.doi.org/10.1016/0741-8329(91)90465-9.

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38

Fortunato, Franco, Xiaoying Deng, Lawrence K. Gates, Craig J. McClain, Daniel Bimmler, Rolf Graf, and David C. Whitcomb. "Pancreatic response to endotoxin after chronic alcohol exposure: switch from apoptosis to necrosis?" American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 2 (February 2006): G232—G241. http://dx.doi.org/10.1152/ajpgi.00040.2005.

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Chronic alcohol consumption is known to increase the susceptibility to acute and chronic pancreatitis, and it is likely that a cofactor is required to initiate the progression to alcoholic pancreatitis. The severity and complications of alcoholic and nonalcoholic acute pancreatitis may be influenced by a number of cofactors, including endotoxemia. To explore the effect of a possible cofactor, we used endotoxin [lipopolysaccharide (LPS)] as a tool to induce cellular injury in the alcoholic pancreas. Single, increasing doses of endotoxin were injected in rats fed an alcohol or control diet and killed 24 h after the injection. We examined the mechanism by which LPS exacerbates pancreatic injury in alcohol-fed rats and whether the injury is associated with apoptosis or necrosis. We showed that chronic alcohol exposure alone inhibits apoptosis through the intrinsic pathway and the downstream apoptosis executor caspase-3 compared with the controls. Pancreatic necrosis and inflammation increased after LPS injection in control and alcohol-fed rats in a dose-dependent fashion but with a significantly greater response in the alcohol-fed animals. Caspase activities and TdT-mediated dUTP nick-end labeling positivity were lower in the alcoholic pancreas injected with LPS, whereas the histopathology and inflammation were more severe compared with the control-fed animals. Assessment of a putative indicator of necrosis, the ratio of ADP to ATP, indicated that alcohol exposure accelerates pancreatic necrosis in response to endotoxin. These findings suggest that the pancreas exposed to alcohol is more sensitive to LPS-induced damage because of increased sensitivity to necrotic cell death rather than apoptotic cell death. Similar to the liver, the pancreas is capable of responding to LPS with a more severe response in alcohol-fed animals, favoring pancreatic necrosis rather than apoptosis. We speculate that this mechanism may occur in acute alcoholic pancreatitis patients.

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39

Gajbhiye, Snehalata V., Raakhi K. Tripathi, Anup Petare, Anirudha V. Potey, and Arun Shankar. "Minocycline in Alcohol Withdrawal Induced Anxiety and Alcohol Relapse in Rats." Current Clinical Pharmacology 13, no. 1 (August 20, 2018): 65–72. http://dx.doi.org/10.2174/1574884713666180228110310.

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40

Mcmillan, D. E., Mi Li, and D. J. Shide. "Differences Between Alcohol-Preferring and Alcohol-Nonpreferring Rats in Ethanol Generalization." Pharmacology Biochemistry and Behavior 64, no. 2 (October 1999): 415–19. http://dx.doi.org/10.1016/s0091-3057(99)00053-2.

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41

Kiefer, Stephen W., and Nancy E. Badia-Elder. "Taste reactivity in high-alcohol-sensitive and low-alcohol-sensitive rats." Alcohol 14, no. 3 (May 1997): 225–29. http://dx.doi.org/10.1016/s0741-8329(96)00146-2.

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42

Badia-Elder, Nancy E., and Stephen W. Kiefer. "Taste Reactivity in Alcohol-Preferring AA and Alcohol-Avoiding ANA Rats." Alcohol 18, no. 2-3 (June 1999): 159–63. http://dx.doi.org/10.1016/s0741-8329(98)00079-2.

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43

Serra, S. "GAMMA-HYDROXYBUTYRIC ACID VERSUS ALCOHOL PREFERENCE IN SARDINIAN ALCOHOL-PREFERRING RATS." Alcohol and Alcoholism 37, no. 2 (March 1, 2002): 128–31. http://dx.doi.org/10.1093/alcalc/37.2.128.

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44

Hansson, Anita C., Anne Koopmann, Stefanie Uhrig, Sina Bühler, Esi Domi, Eva Kiessling, Roberto Ciccocioppo, et al. "Oxytocin Reduces Alcohol Cue-Reactivity in Alcohol-Dependent Rats and Humans." Neuropsychopharmacology 43, no. 6 (November 1, 2017): 1235–46. http://dx.doi.org/10.1038/npp.2017.257.

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45

Kiefer, Stephen W., Nancy Badia-Elder, and Paula J. Bice. "Taste Reactivity in High Alcohol Drinking and Low Alcohol Drinking Rats." Alcoholism: Clinical and Experimental Research 19, no. 2 (April 1995): 279–84. http://dx.doi.org/10.1111/j.1530-0277.1995.tb01503.x.

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46

Ishigami, M., T. Ohnishi, M. Eguchi, S. Mizuiri, and A. Hasegawa. "Renal effects of alcohol withdrawal in five-week alcohol-treated rats." Journal of Studies on Alcohol 58, no. 4 (July 1997): 392–96. http://dx.doi.org/10.15288/jsa.1997.58.392.

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47

Alaux-Cantin, Stéphanie, Romain Buttolo, Hakim Houchi, Jérôme Jeanblanc, and Mickaël Naassila. "Memantine reduces alcohol drinking but not relapse in alcohol-dependent rats." Addiction Biology 20, no. 5 (August 20, 2014): 890–901. http://dx.doi.org/10.1111/adb.12177.

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Perfumi, M., C. Polidori, P. L. Pompei, G. De Caro, and M. Massi. "The tachykinin NH2-senktide inhibits alcohol intake in alcohol-preferring rats." Pharmacology Biochemistry and Behavior 38, no. 4 (April 1991): 881–87. http://dx.doi.org/10.1016/0091-3057(91)90257-3.

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49

Lê, A. D., A. Wang, S. Harding, W. Juzytsch, and Y. Shaham. "Nicotine increases alcohol self-administration and reinstates alcohol seeking in rats." Psychopharmacology 168, no. 1-2 (January 21, 2003): 216–21. http://dx.doi.org/10.1007/s00213-002-1330-9.

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50

Rowland, Neil E., and Kenneth R. Morian. "Effect of dexfenfluramine on alcohol intake in alcohol-preferring “P” rats." Alcohol 9, no. 6 (November 1992): 559–61. http://dx.doi.org/10.1016/0741-8329(92)90097-t.

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