LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway
LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway作者机构：Department of GastroenterologyThe First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina Clinical Research Center for Hepatobiliary and Pancreatic Diseases of Zhejiang ProvinceHangzhou 310003Zhejiang ProvinceChina
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2019年第25卷第45期
页 面：6607-6618页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：LB100 Nonalcoholic fatty liver disease Serine/threonine-protein phosphatase 2A Lipid metabolism AMP-activated protein kinaseα Sirtuin 1
摘 要：BACKGROUND It is well known that nonalcoholic fatty liver disease(NAFLD)is associated with insulin resistance(IR).LB100,a serine/threonine protein phosphatase 2A(PP2A)inhibitor,is closely related to ***,there is little data regarding its direct influence on *** To elucidate the effect and underlying mechanism of LB100 in *** After 10 wk of high fat diet(HFD)feeding,male C57BL/6 mice were injected intraperitoneally with vehicle or LB100 for an additional 6 wk(three times a week).The L02 cell line was treated with LB100 and free fatty acids(FFAs)for 24 *** and eosin and oil red O staining were performed for histological *** blot analysis was used to detect the protein expression of Sirtuin 1(Sirt1),total and phosphorylated AMP-activated protein kinaseα(AMPKα),and the proteins involved in lipogenesis and fatty acid *** mRNA levels were determined by *** inhibition of AMPK was performed to further examine the exact mechanism of LB100 in *** LB100 significantly ameliorated HFD-induced obesity,hepatic lipid accumulation and hepatic injury in *** addition,LB100 significantly downregulated the protein levels of acetyl-CoA carboxylase,sterol regulatory element-binding protein 1 and its lipogenesis target genes,including stearoyl-CoA desaturase-1 and fatty acid synthase,and upregulated the levels of proteins involved in fatty acidβ-oxidation,such as peroxisome proliferator-activated receptorα(PPARα),peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α),carnitine palmitoyltransferase 1α,acyl-CoA oxidase 1 and uncoupling protein 2,as well as the upstream mediators Sirt1 and AMPKαin the livers of HFD-fed *** vitro,LB100 alleviated FFA-induced lipid accumulation in L02 cells through the AMPK/Sirt1 signaling *** studies showed that the curative effect of LB100 on lipid accumulation was abolished by inhibiting AMPKαin L02 *** PP2A inhibition by LB
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