Chen Jing, Liu Jie, Wang Ye, Hu Xuemei, Zhou Feng, Hu Yimeng, Yuan Yin, Xu Yancheng
Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China; Department of Integrated Wards, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.
Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.
Biomed Pharmacother. 2017 Jul;91:621-631. doi: 10.1016/j.biopha.2017.04.125. Epub 2017 May 6.
Wogonin has been reported to attenuate hyperglycemia in diabetic mice via anti-adipogenic effect on adipocytes. The potential therapeutic role of wogonin in nonalcoholic fatty liver disease (NAFLD) remains obscure. The aim of the present study was to explore the protective effect of wogonin on NAFLD mice and cultured NCTC 1469 cells exposed to palmitate. Wogonin supplementation significantly improved metabolic parameters in NAFLD mice, including body weight, blood glucose, insulin resistance, adiponectin, blood lipids, aminotransferases and hepatic histopathology. Further research in liver tissues from NAFLD mice and NCTC 1469 cells stressed by lipotoxicity showed wogonin treatment reduced inflammatory response by lowering interleukin-6 (IL-6) and tumor necrosis factor α (TNFα), alleviated oxidative stress by preventing the accumulation of oxidative product malondialdehyde (MDA) and strengthening the anti-oxidative capacity of glutathione (GSH), Superoxide Dismutase (SOD) and Glutathione Peroxidase (GPX). In addition, wogonin repaired the lipotoxicity-induced decline of peroxisome proliferator- activated receptor α (PPARα) and adiponectin receptor 2 (AdipoR2) in hepatocytes, in vivo and in vitro. Knock-down of PPARα abolished the protective effect of wogonin on NCTC 1469 cells, including the up-regulation of AdipoR2. Taken together, the current study demonstrated wogonin might be a potential therapeutic agent for NAFLD via up-regulation of hepatic PPARα/AdipoR2.
据报道，汉黄芩素可通过对脂肪细胞的抗脂肪生成作用减轻糖尿病小鼠的高血糖症。汉黄芩素在非酒精性脂肪性肝病（NAFLD）中的潜在治疗作用仍不清楚。本研究的目的是探讨汉黄芩素对NAFLD小鼠和暴露于棕榈酸的培养NCTC 1469细胞的保护作用。补充汉黄芩素可显著改善NAFLD小鼠的代谢参数，包括体重、血糖、胰岛素抵抗、脂联素、血脂、氨基转移酶和肝脏组织病理学。对NAFLD小鼠肝脏组织和受脂毒性应激的NCTC 1469细胞的进一步研究表明，汉黄芩素治疗可通过降低白细胞介素-6（IL-6）和肿瘤坏死因子α（TNFα）来减轻炎症反应，通过防止氧化产物丙二醛（MDA）的积累和增强谷胱甘肽（GSH）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPX）的抗氧化能力来减轻氧化应激。此外，汉黄芩素在体内和体外修复了脂毒性诱导的肝细胞中过氧化物酶体增殖物激活受体α（PPARα）和脂联素受体2（AdipoR2）的下降。敲低PPARα消除了汉黄芩素对NCTC 1469细胞的保护作用，包括AdipoR2的上调。综上所述，本研究表明汉黄芩素可能通过上调肝脏PPARα/AdipoR2成为NAFLD的潜在治疗药物。
