文献类型：期刊文献

英文题名：Therapeutic Effect of Puerarin on Non-Alcoholic Rat Fatty Liver by Improving Leptin Signal Transduction through JAK2/STAT3 Pathways

作者：Zheng, Peiyong[1];Ji, Guang[1];Ma, Zansong[1];Liu, Tao[1];Xin, Lianjun[1];Wu, Hongzhong[2];Liang, Xin[2];Liu, Jianwen[2]

机构：[1]Shanghai Univ Tradit Chinese Med, Longhua Hosp, Inst Digest Dis, Shanghai 200032, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai 200237, Peoples R China

年份：2009

卷号：37

期号：1

起止页码：69

外文期刊名：AMERICAN JOURNAL OF CHINESE MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000263679300007)】；

基金：The authors are grateful for the financial supports from the E-institutes of Shanghai Municipal Education Commission, Project No. E03008; Shanghai Leading Academic Discipline Project No. J50305; and the National Science Foundation of China, Project Nos. 30572380 and 30772802.

语种：英文

外文关键词：Puerarin; Non alcoholic Fatty Disease; Leptin; Leptin Resistance; P-JAK2/P-STAT3

摘要：In order to investigate the mechanism of the therapeutic effect of puerarin on non-alcoholic fatty liver disease, a non-alcoholic fatty disease male rat model was induced by a high fat diet, all rats were randomly divided into a blank group, model group, simavastatin group and puerarin group. After 4 weeks of drug treatment, the liver was slided to investigate pathological morphology. Elisa was used to measure the total cholesterol (TC), triglyeride (TG) in liver, and leptin content in serum. RT-PCR and Western blotting were employed to detect liver leptin mRNA receptor expression and P-JAK2, P-STAT3 expression levels in the liver respectively. The results showed that puerarin significantly decreased the TG, TC content in liver of the non-alcoholic fatty disease rats, ameliorated steatosis in liver, lowered liver inflammatory reaction, decreased leptin level in serum, and enhanced the expression of leptin receptor mRNA and P-JAK2/P-STAT3 level. All the results demonstrated that puerarin can exhibit therapeutic effect on non-alcoholic fatty liver disease by improving leptin signal transduction through JAK2/STAT3 pathways.