Effect of aloe emodin on the treatment of nonalcoholic steatohepatitis mice
ZHANG Ying-ying1, ZHOU Pei1, WANG Bing-fang2
(1. School of Medicine, Jiangsu University, Zhenjiang Jiangsu 212013; 2. Department of Gastroenterology, Affiliated Kunshan Hospital of Jiangsu University, Kunshan Jiangsu 215300, China)
Abstract:[Abstract]Objective: To investigate the role of traditional Chinese medicine monomer aloe emodin(AE) in treatment of nonalcoholic steatohepatitis(NASH). Methods: Kunming mice were fed with low protein and high fat diet for 8 weeks to establish the NASH mouse model. Then the mice were randomly divided into NASH model group,lowdose AE group, middledose AE group,highdose AE group,anetholtrithione group,which of them were given physiological saline, various doses of AE or anetholtrithione group for 4 weeks. General conditions of the animals were observed, before the mice were executed at the end of week 12.The serum alanine aminotransferase(ALT) activity, aspartate aminotransferase(AST) activity, serum triglyceride(TG) activity, serum superoxide dismutase(SOD) levels, serum malondialdehyde(MDA)levels, serum endotoxin levels, serum tumor necrosis factorα(TNFα)levels were determined. The liver tissue were prepared to investigate hepatic pathologic structure by hematoxylin and eosin(HE) staining. Results:Compared to the NASH model group,AE at different doses all could significantly reduce serum ALT, AST, TG, endotoxin, MDA and TNFα level(P<0.01),increase serum SOD activity significantly. The effect of AE high dose group was the best and similar with anetholtrithione group(P>0.05). The pathological observation showed that AE could obviously relieve the hepatocyte steatosis, inflammatory infiltration and other pathological changes. Conclusion: AE exerts the clear effect on the treatment of NASH via improving liver function, lipid metabolism, relieving liver fatty degeneration and inflammatory infiltration.
[1]张彦文.龙牙肝泰胶囊治疗非酒精性脂肪肝62例的临床观察\[J\].中医药信息,2014,31(1):91-92.[2]Paschos P,Paletas K. Non alcoholic fatty liver disease and metabolic syndrome\[J\]. Hippokratia, 2009,13(1):9-19.[3]施军平,范建高.保肝抗炎药物在非酒精性脂肪性肝病治疗中的作用[J].世界临床药物,2010,31(9):526-529,537.[4]罗霄山.芦荟大黄素对CCl4损伤原代培养大鼠肝细胞的保护作用\[J\].中医药学刊,2003,21(7):1101-1102.[5]许丹,周巍,于洪刚,等.芦荟大黄素对血吸虫病性肝纤维化小鼠的影响\[J\].中西医结合肝病杂志,2012,22(2):107-109[6]刘贺荣,李国莉,任彬彬,等.非酒精性脂肪肝动物模型的建立\[J\].宁夏医科大学学报,2010,32(8):934-937.[7]董姝,刘平,孙明瑜.非酒精性脂肪肝发病机制:“二次打击学说”研究进展\[J\].临床肝胆病杂志,2012,28(7):551-555.[8]Fan JG,Farrell GC.Epidemiology of nonalcoholic fatty liver disease in china\[J\].J Hepatol,2009,50(1):204-210.[9]VarelaRey M,Embade N,Ariz U, et al. Nonalcoholic steatohepatitis and animal models: understanding the human disease\[J\].Int J Biochem Cell Biol,2009,41(5): 969-976.[10]Day CP,James OF.Steatohepatitis:a tale of two“hits”?\[J\].Gastroenterology,1998,114(4):842-845.[11]Starley BQ,Calcagno CJ,Harrison SA,et al.Nonalcoholic fatty liver disease and hepatocellular carcinoma:a weighty connection\[J\].Hepatology,2010,51(5):1820-1832.[12]Verbeek J, Cassiman D, Lannoo M, et al.Treatment of nonalcoholic fatty liver disease: can we already face the epidemic?\[J\]. Acta Gastroenterol Belg,2013,76(2): 200-209.[13]刘菲,钟岚,王军臣.茴三硫防治非酒精性脂肪性肝炎的实验研究\[J\].中华消化杂志, 2002,22(9):532-534.[14]Clark JM,Brancati FL,Dichl AM.The prevalence and etiology of elevated aminotransferase levels in the United States\[J\]. Am J Gastroenterol,2003,98(5):960-967.[15]Chiarpotto E, Castello L, Leonarduzzi G,et al. Role of 4hydroxy2,3nonenal in the pathogenesis of fibrosis\[J\]. Biofactors,2005, 24(1/4): 229-236.[16]FernándezSánchez A, MadrigalSantillán E, Bautista M, et al.Inflammation,oxidative stress,and obesity\[J\].Int J Mol Sci,2011,12(5):3117-3132.[17]Bigorgne AE,BouchetDelbos L,Naveau S,et al.Obesityinduced lymphocyte hyperresponsiveness to chemokines: a new mechanism of Fatty liver inflammation in obese mice\[J\].Gastroenterology,2008,134(5):1459-1469.[18]张晓艳,韩德五,许瑞龄,等. 蔗糖在促进大鼠非酒精性脂肪性肝炎形成及发展中的作用\[J\]. 山西医科大学学报,2008,39(6):497-500.[19]Farhadi A,Gundlapalli S,Shaikh M,et al.Susceptibility to gut leakiness: a possible mechanism for endotoxaemia in nonalcoholic steatohepatitis\[J\].Liver Int,2008,28(7):1026-1033.