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人参皂苷 Rb1 通过过氧化物酶体增殖物激活受体减轻高脂饮食诱导的肝细胞凋亡。

Ginsenoside Rb1 Alleviated High-Fat-Diet-Induced Hepatocytic Apoptosis via Peroxisome Proliferator-Activated Receptor .

机构信息

Department of Endocrinology, First Affiliated Hospital of Jinzhou Medical University, China.

Department of Pharmacy, Taikang Xianlin Drum Tower Hospital, Medical School of Nanjing University, China.

出版信息

Biomed Res Int. 2020 Jul 13;2020:2315230. doi: 10.1155/2020/2315230. eCollection 2020.

Abstract

OBJECTIVE

High-fat-diet- (HFD-) induced hepatic cell apoptosis is common in mice with nonalcoholic fatty liver disease (NAFLD). We aim to investigate the effect of Ginsenoside Rb1 (GRb1) on hepatocyte apoptosis.

METHODS

C57BL/6J mice with HFD were used to induce a liver-injured model with cell apoptosis. In addition, GRb1 was used to treat HFD-induced apoptosis in a liver with or without inhibitor of peroxisome proliferator-activated receptor (PPAR-).

RESULTS

Compared with C57BL/6J mice with common chow, there are downregulated PPAR- but upregulated cell apoptosis in the liver of mice with HFD. Furthermore, GRb1 elevated the hepatic PPAR- level and suppressed hepatocytic apoptosis. However, GW9662 abolished the effects of GRb1 on apoptosis in the liver.

CONCLUSIONS

GRb1 alleviated HFD-induced apoptosis of hepatocytes of mice via PPAR-.

摘要

目的

高脂肪饮食(HFD)诱导的肝细胞凋亡在非酒精性脂肪性肝病(NAFLD)小鼠中很常见。本研究旨在探讨人参皂苷 Rb1(GRb1)对肝细胞凋亡的影响。

方法

采用 C57BL/6J 小鼠的高脂肪饮食诱导肝损伤模型伴细胞凋亡,同时用 GRb1 处理或不处理过氧化物酶体增殖物激活受体(PPAR-)抑制剂诱导的 HFD 诱导的肝凋亡。

结果

与普通饲料喂养的 C57BL/6J 小鼠相比,高脂肪饮食喂养的小鼠肝脏中 PPAR-表达下调,细胞凋亡增加。此外,GRb1 可提高肝组织中 PPAR-水平,抑制肝实质细胞凋亡。然而,GW9662 可消除 GRb1 对肝组织细胞凋亡的作用。

结论

GRb1 通过 PPAR-减轻 HFD 诱导的小鼠肝细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c4/7376403/7f8cc67eb1db/BMRI2020-2315230.001.jpg

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