Indole alkaloids of Alstonia scholaris (L.) R. Br. alleviated nonalcoholic fatty liver disease in mice fed with high-fat diet

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作者
Shui-Fen Sun
Hui-Jie Zhong
Yun-Li Zhao
Xiu-Ying Ma
Jin-Bo Luo
Ling Zhu
Yu-Ting Zhang
Wen-Xue Wang
Xiao-Dong Luo
Jia-Wei Geng
机构
[1] Affiliated Hospital of Kunming University of Science and Technology,Department of Infectious Disease and Hepatic Disease, First People’s Hospital of Yunnan Province
[2] Kunming University of Science and Technology,School of Medicine
[3] Kunming University of Science and Technology,Faculty of Life Science and Technology
[4] Kunming Institute of Botany,State Key Laboratory of Phytochemistry and Plant Resources in West China
[5] Chinese Academy of Sciences,undefined
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Hepatic disease; Hepatic lipogenesis; Fatty acid oxidation;
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摘要
Alstonia scholaris (L.) R. Br (Apocynaceae) is a well-documented medicinal plant for treating respiratory diseases, liver diseases and diabetes traditionally. The current study aimed to investigate the effects of TA on non-alcoholic fatty liver disease (NAFLD). A NAFLD model was established using mice fed a high-fat diet (HFD) and administered with TA (7.5, 15 and 30 mg/kg) orally for 6 weeks. The biochemical parameters, expressions of lipid metabolism-related genes or proteins were analyzed. Furthermore, histopathological examinations were evaluated with Hematoxylin–Eosin and MASSON staining. TA treatment significantly decreased the bodyweight of HFD mice. The concentrations of low-density lipoprotein (LDL), triglyceride (TG), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were also decreased significantly in TA-treated mice group, accompanied by an increase in high-density lipoprotein (HDL). Furthermore, TA alleviated hepatic steatosis injury and lipid droplet accumulation of liver tissues. The liver mRNA levels involved in hepatic lipid synthesis such as sterol regulatory element-binding protein 1C (SREBP-1C), regulators of liver X receptor α (LXRα), peroxisome proliferator activated receptor (PPAR)γ, acetyl-CoA carboxylase (ACC1) and stearyl coenzyme A dehydrogenase-1 (SCD1), were markedly decreased, while the expressions involved in the regulation of fatty acid oxidation, PPARα, carnitine palmitoyl transterase 1 (CPT1A), and acyl coenzyme A oxidase 1 (ACOX1) were increased in TA-treated mice. TA might attenuate NAFLD by regulating hepatic lipogenesis and fatty acid oxidation.
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