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作者

Xiaoling Li, Mengjiao Yang, Hang Sun, Md Reyad Ul Ferdous, Ling Gao, Jiajun Zhao, Yongfeng Song

作者单位

Department of Endocrinology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250021, China Shandong Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong, 250021, China Shandong Prevention and Control Engineering Laboratory of Endocrine and Metabolic Diseases, Jinan, Shandong, 250021, China. Electronic address: jjzhao@sdu.edu.cn. Shandong Prevention and Control Engineering Laboratory of Endocrine and Metabolic Diseases, Jinan, Shandong, 250021, China Shandong Clinical Research Center of Diabetes and Metabolic Diseases, Jinan, Shandong, 250021, China Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China Affiliations Shandong Institute of Endocrine & Metabolic Diseases, Jinan, China. Electronic address: syf198506@16 Shandong Prevention and Control Engineering Laboratory of Endocrine and Metabolic Diseases, Jinan, Shandong, 250021, China. com.

刊名

Biochemical and biophysical research communications

年份

2022

卷号

Vol.594

页码

168-176

ISSN

1090-2104

关键词

CypD Fibrosis Inflammation NASH Steatosis.

摘要

Cyclophilin D can stimulate the opening of the membrane permeability transition pore and regulate mitochondrial function. Whole-body knockout of CypD improved high fat diet-induced hepatic steatosis by reducing the excess opening of the mPTP and lipid deposition. However, whether CypD significantly ameliorates nonalcoholic steatohepatitis has not been studied. Therefore, we established liver-specific CypD knockout mice and fed a HFHC diet to induce NASH. Compared with the wild-type mice, the...更多

Cyclophilin D can stimulate the opening of the membrane permeability transition pore and regulate mitochondrial function. Whole-body knockout of CypD improved high fat diet-induced hepatic steatosis by reducing the excess opening of the mPTP and lipid deposition. However, whether CypD significantly ameliorates nonalcoholic steatohepatitis has not been studied. Therefore, we established liver-specific CypD knockout mice and fed a HFHC diet to induce NASH. Compared with the wild-type mice, the CypD LKO not only showed improved lipid deposition and insulin resistance by increasing fatty acid oxidation but also displayed ameliorated hepatic inflammation, although the symptoms of fibrosis in the NASH model were not significantly improved. In addition, we used bile duct ligation or a 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet to induce cholestatic disease and found that CypD LKO had also no significant effect on acute fibrosis. Thus, CypD LKO can inhibit the progression of early NASH by ameliorating steatosis and inflammatory symptoms. These results suggest a new strategy for the treatment of early NASH.收起

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期刊