The protective effect of tea polyphenols on chronic alcoholic liver injury in rats

doi:10.12047/j.cjap.5708.2018.107

Abstract

Abstract: Objective: To investigate the protective effects and potential mechanisms of tea polyphenols intervention on excess alcohol intake induced liver injury in rats. This study established the animal model of chronic liver injury rats induced by alcohol. Our results will provide experimental evidence for the effects of tea polyphenol on chronic alcoholic liver injury. Methods: Alcohol-induced liver injury rat models were established, and the tea polyphenols intervention was performed in the meantime. After 8 weeks, rats were anesthetized, and visceral fat and liver samples were separated, weighted and stored. Visceral fat content was evaluated in fat/body weight ratio. Liver lipid accumulation was assessed by liver index and the result of Oil Red O staining. Hepatic superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, total antioxidant capacity assay (T-AOC) and glutathione peroxidase (GSH-Px) activity were detected. And fatty acid translocase (FAT/CD36) protein level in liver was detected. Results: Compared with the control group rats, the fat/body weight ratio, SOD/MDA, T-AOC and GSH-Px activity of chronic liver injury rats were decreased significantly (P<0.05,P<0.01). Meanwhile the liver index, FAT/CD36 protein level and lipid deposition in liver of chronic liver injury rats were increased (P<0.01). Compared with chronic liver injury rats, the tea polyphenols intervention increased fat/body weight ratio (P<0.05), and significantly increased SOD/MDA, T-AOC and GSH-Px activity (P<0.01). Meanwhile the tea polyphenols intervention reduced liver index (P<0.01), FAT/CD36 protein level (P<0.01) and lipid deposition in liver. Conclusion: Tea polyphenols intervention can improve lipid deposition and oxidative stress in chronic alcoholic liver, which is concurrent with decreased FAT/CD36 protein expression on the hepatocyte membrane.

Key words: alcohol, liver injury, tea polyphenols, lipid accumulation, oxidative stress, FAT/CD36, rat

ZHANG Yong, LI Miao-miao, HUA Tian-miao, SUN Qing-yan. The protective effect of tea polyphenols on chronic alcoholic liver injury in rats[J]. CJAP, 2018, 34(6): 481-484.

References

[1] Ge N, Liang H, Liu Y, et al. Protective effect of Aplysin on hepatic injury in ethanol-treated rats[J]. Food Chem Toxicol, 2013, 62:361-372.
[2] Pang M, de la Monte SM, Longato L, et al. PPARdelta agonist attenuates alcohol-induced hepatic insulin resistance and improves liver injury and repair[J]. J Hepatol, 2009, 50(6):1192-1201.
[3] Li YM, Zhang XG, Zhou HL, et al. Effects of tea polyphenols on hepatic fibrosis in rats with alcoholic liver disease[J]. Hepatobiliary Pancreat Dis Int, 2004, 3(4):577-579.
[4] 张宇, 陈韶华, 张幸国, 等. 茶多酚治疗慢性酒精性肝损伤的实验研究[J].中华肝脏病杂志, 2005, 13(2):125-127.
[5] Ji C. Advances and new concepts in alcohol-induced organelle stress, unfolded protein responses and organ damage[J]. Biomolecules, 2015, 5(2):1099-1121.
[6] 罗艳蕊, 王建设, 崔迪. 茶多酚对营养性肥胖大鼠肝脏自由基代谢的影响[J]. 中国应用生理学杂志, 2012, 28(3):196-198.
[7] Fei Q, Gao Y, Zhang X, et al. Effects of Oolong tea polyphenols, EGCG, and EGCG3 Me on pancreatic alpha-amylase activity in vitro[J]. J Agric Food Chem, 2014, 62(39):9507-9514.
[8] Tao J, Shen X, Ai Y, et al. Tea polyphenols protect against ischemia/reperfusion-induced liver injury in mice through anti-oxidative and anti-apoptotic properties[J]. Exp Ther Med, 2016, 12(5):3433-3439.
[9] Kim JY, van de Wall E, Laplante M, et al. Obesity-associated improvements in metabolic profile through expansion of adipose tissue[J]. J Clin Invest, 2007, 117(9):2621-2637.
[10] Zhou SL, Gordon RE, Bradbury M, et al. Ethanol up-regulates fatty acid uptake and plasma membrane expression and export of mitochondrial aspartate aminotransferase in HepG2 cells[J]. Hepatology, 1998, 27(4):1064-1074.
[11] Kang L, Chen X, Sebastian BM, et al. Chronic ethanol and triglyceride turnover in white adipose tissue in rats:inhibition of the anti-lipolytic action of insulin after chronic ethanol contributes to increased triglyceride degradation[J]. J Biol Chem, 2007, 282(39):28465-28473.
[12] Cusi K. The role of adipose tissue and lipotoxicity in the pathogenesis of type 2 diabetes[J]. Curr Diab Rep, 2010, 10(4):306-315.
[13] Zhang Y, Kallenberg C, Hyatt HW, et al. Change in the lipid transport capacity of the liver and blood during reproduction in rats[J]. Front Physiol, 2017, 8:517.
[14] Glatz JFC, Luiken JFP. Dynamic role of the transmembrane glycoprotein CD36(SR-B2) in cellular fatty acid uptake and utilization[J]. J Lipid Res, 2018, 59(7):1084-1093.
[15] Martius G, Alwahsh SM, Rave-Frank M, et al. Hepatic fat accumulation and regulation of FAT/CD36:an effect of hepatic irradiation[J]. Int J Clin Exp Pathol, 2014, 7(8):5379-5392.
[16] Yang J, Sambandam N, Han X, et al. CD36 deficiency rescues lipotoxic cardiomyopathy[J]. Circ Res, 2007, 100(8):1208-1217.
[17] Kang X, Zhong W, Liu J, et al. Zinc supplementation reverses alcohol-induced steatosis in mice through reactivating hepatocyte nuclear factor-4alpha and peroxisome proliferator-activated receptor-alpha[J]. Hepatology, 2009, 50(4):1241-1250.
[18] 肖敏, 刘重斌, 孙未, 等. 补锌对酒精性肝病的影响及其分子机制[J]. 中国应用生理学杂志, 2012, 28(1):84-88.
[19] Storch J, Thumser AE. The fatty acid transport function of fatty acid-binding proteins[J]. Biochim Biophys Acta, 2000, 1486(1):28-44.