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（桑植）生物碱减轻小鼠高脂饮食诱导的肥胖和非酒精性脂肪性肝病。

(Sangzhi) Alkaloids Alleviate High-Fat Diet-Induced Obesity and Nonalcoholic Fatty Liver Disease in Mice.

作者信息

Chen Yan-Min, Lian Chun-Fang, Sun Qian-Wen, Wang Ting-Ting, Liu Yuan-Yuan, Ye Jun, Gao Li-Li, Yang Yan-Fang, Liu Shuai-Nan, Shen Zhu-Fang, Liu Yu-Ling

机构信息

Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.

出版信息

Antioxidants (Basel). 2022 May 5;11(5):905. doi: 10.3390/antiox11050905.

DOI:10.3390/antiox11050905
PMID:35624769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9137915/
Abstract

Nonalcoholic fatty liver disease (NAFLD), obesity, and type 2 diabetes mellitus (T2DM) have highly related mechanisms. (Sangzhi) alkaloids (SZ-A) from L. were approved in 2020 for the treatment of T2DM. In this study, we examined the therapeutic effects and mechanism of SZ-A on obesity and NAFLD in mice. Mice (C57BL/6J) fed a high-fat diet (HFD) for 14 weeks were treated with SZ-A for another 6 weeks. HFD-induced weight gain was reduced by SZ-A in a dose-dependent manner. SZ-A treatment significantly stimulated adiponectin expression and secretion in adipose tissue and 3T3-L1 adipocytes. Additionally, SZ-A markedly reduced hepatic steatosis (triglyceride, total cholesterol) and expression of pro-inflammatory and pro-fibrotic genes. SZ-A regulated lipid metabolism and oxidative stress (malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH)) in the liver. Palmitic acid-induced insulin resistance and lipid accumulation in HepG2 cells were also repressed by SZ-A. Collectively, SZ-A protected mice from HFD-induced NAFLD through an indirect effect of improved systemic metabolism reducing bodyweight, and a direct effect by enhancing the lipid metabolism of HepG2 cells. The weight-loss effect of SZ-A in mice was partly due to improved fatty oxidation instead of influencing food consumption.

摘要

非酒精性脂肪性肝病（NAFLD）、肥胖症和2型糖尿病（T2DM）具有高度相关的机制。来自[植物名称未给出]的（桑枝）生物碱（SZ-A）于2020年被批准用于治疗T2DM。在本研究中，我们研究了SZ-A对小鼠肥胖症和NAFLD的治疗效果及机制。给喂食高脂饮食（HFD）14周的小鼠（C57BL/6J）再用SZ-A治疗6周。SZ-A以剂量依赖性方式减轻了HFD诱导的体重增加。SZ-A治疗显著刺激了脂肪组织和3T3-L1脂肪细胞中脂联素的表达和分泌。此外，SZ-A显著降低了肝脏脂肪变性（甘油三酯、总胆固醇）以及促炎和促纤维化基因的表达。SZ-A调节了肝脏中的脂质代谢和氧化应激（丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽（GSH））。SZ-A还抑制了棕榈酸诱导的HepG2细胞中的胰岛素抵抗和脂质积累。总体而言，SZ-A通过改善全身代谢减轻体重的间接作用以及增强HepG2细胞脂质代谢的直接作用，保护小鼠免受HFD诱导的NAFLD。SZ-A在小鼠中的减肥作用部分归因于脂肪酸氧化改善而非影响食物消耗。

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