Experimental study on the improvement of non-alcoholic fatty liver disease by regulating G0S2 and ATGL expression with polydatin
10.19405/j.cnki.issn1000-1492.2025.10.010
- VernacularTitle:虎杖苷通过调节 G0S2 和 ATGL 表达改善 非酒精性脂肪肝病的研究
- Author:
Luguang Sheng
1
;
Dandan Liu
2
;
Weibin Liu
2
;
Tao Lei
2
;
Qingguang Chen
3
;
Hao Lu
3
;
Bilin Xu
4
Author Information
1. Shanghai Putuo Central School of Clinical Medicine , Anhui Medical University, Shanghai 200062 ; The Fifth School of Clinical Medicine , AnhuiMedical University, Hefei 230032
2. Dept of Endocrinology, Putuo Hospital , Shanghai University of Traditional Chinese Medicine , Shanghai 200062
3. Dept of Endocrinology, Shuguang Hospital Afiliated to Shanghai University of Traditional Chinese Medicine , Shanghai 200021
4. Shanghai Putuo Central School of Clinical Medicine , Anhui Medical University, Shanghai 200062 ; The Fifth School of Clinical Medicine , AnhuiMedical University, Hefei 230032;Dept of Endocrinology, Putuo Hospital , Shanghai University of Traditional Chinese Medicine , Shanghai 200062
- Publication Type:Journal Article
- Keywords:
polydatin;
non-alcoholic fatty liver disease;
C57BL/6J mice;
HepG2 cells;
fat decomposition;
G_0/G_1 switch gene 2;
adipose triglyceride lipase
- From:
Acta Universitatis Medicinalis Anhui
2025;60(10):1847-1856
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of polydatin on a high-fat diet-induced non-alcoholic fatty liver disease(NAFLD) mouse model and hepatoma G2(HepG2) cell model, and to reveal its potential molecular mechanisms.
Methods:Thirty 6-week-old male SPF C57BL/6J mice were randomly divided into a normal diet group and a high-fat diet group. After the NAFLD mouse model was established in the high-fat diet group, they were further divided into a model group and a polydatin treatment group. The polydatin treatment group was administered polydatin by gavage at a dose of 250 mg/(kg·d) for 10 weeks, during which body weight was monitored and oral glucose and insulin tolerance tests were performed. At the end of the experiment, a series of tests to evaluate the effects of polydatin on mouse liver weight, blood lipids, liver lipid accumulation, and liver injury markers were performed. The expression of G0/G1 switch gene 2(G0S2) and adipose triglyceride lipase(ATGL) was measured by qRT-PCR and Western blot, and gene expression was further verified using immunohistochemical staining. The effects of polydatin on HepG2 cell activity was assessed by CCK-8 assay, lipid accumulation was observed by oil red O staining, and the expression of G0S2 and ATGL was detected by qRT-PCR and Western blot.
Results:Polydatin significantly reduced the body weight, liver weight, and serum and liver tissue levels of aspartate aminotransferase(AST), alanine aminotransferase(ALT), triglyceride(TG), and total cholesterol (TC) in mice (P < 0. 05) , al⁃leviated pathological liver damage , decreased G0S2 expression (P < 0. 05) , and increased ATGL expression (P <0. 05) . At the cellular level , polydatin reduced lipid droplet accumulation , improved lipid metabolism , decreased G0S2 expression ( P < 0. 05 ) , and increased ATGL expression ( P < 0. 05 ) . Even in cells with knockdown of G0S2 , polydatin still promoted fat decomposition (P < 0. 01) .
Conclusion:Polydatin promotes hepatic fat break⁃down by regulating the expression of G0S2 and ATGL , helping to alleviate metabolic disorders and liver damage in the NAFLD mouse model caused by a high⁃fat diet , offering a new strategy for treating NAFLD.
- Full text:2026030821514011571虎杖苷通过调节G0S2和ATGL表达改善非酒精性脂肪肝病的研究_盛鲁光.pdf
