Mechanism of Kinsenoside in alcoholic liver injury in mice
10.12206/j.issn.2097-2024.202309030
- VernacularTitle:金线莲苷对小鼠酒精性肝损伤的作用机制研究
- Author:
Wenyu HU
1
;
Wenjun SHI
2
;
Xuewu WANG
3
;
Shuoshuo LI
1
Author Information
1. School of Life Science, Beijing University of Chinese Medicine, Beijing 100105, China;Institute of Military Cognition and Brain Sciences, Academy of Military Medical Science, Beijing 100850, China.
2. Institute of Military Cognition and Brain Sciences, Academy of Military Medical Science, Beijing 100850, China;Center on Translational Neuroscience, College of Life & Environmental Science, Minzu University of China, Beijing 100081, China.
3. Lanling County Skin Disease Prevention Station of Shandong Province, Linyi 277700, China.
- Publication Type:Originalarticles
- Keywords:
kinsenoside;
alcoholic liver injury;
lipid deposition;
PPARα;
SREBP1
- From:
Journal of Pharmaceutical Practice and Service
2026;44(1):12-19
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and potential mechanism of kinsenoside （KD）-the main ingredient of Anoectochilus roxburghii （AR） on alcoholic liver injury in mouse models of chronic and acute alcoholic liver injury, and provide a theoretical basis for the development of drugs for alcoholic liver injury. Methods Chronic and acute alcoholic liver injury mouse models were induced by feeding liquid diet containing 30% alcohol and gavage of high doses of alcohol （6 g/kg）, respectively. The KD （50 mg/kg） and AR （250 mg/kg） were administrated by intragastric administration. Body weight, liver index, serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST） levels, serum total triglyceride （TG） and cholesterol （TC） levels were measured; hematoxylin-eosin and oil red O staining was performed on liver tissues; lipid metabolic related genes （PPARα and SREBP1） expression levels were detected by QPCR. Results Both models of alcoholic liver injury resulted in increased hepatic transaminase activity and elevated lipids, accompanied by massive vacuolar structure and lipid droplet formation in pathological liver sections. In the chronic alcoholic liver injury model, ALT and AST were significantly reduced after KD or AR treatment （P<0.05, P<0.001）; the transcriptional activity of SREBP1 was significantly reduced after KD or AR treatment （P<0.01, P<0.05）. In the acute alcoholic liver injury model, AST was significantly reduced after KD or AR treatment （P<0.01, P<0.01）, and TG level was significantly decreased （P<0.01, P<0.01）. Conclusion KD, as the main active ingredient of AR, played a major role in hepatoprotection in mice. KD treatment significantly alleviated chronic and acute alcoholic liver injury and reduced the lipid deposition in liver; KD promoted lipolysis by increasing PPARα and inhibiting the expression of SREBP1 to reduce the synthesis and accumulation of lipids, thus exerting its role in regulating lipid metabolism, which suggested that KD, as the active ingredient of AR, could be a potential drug for the treatment of ALD.
