Experimental study of Lentinan antagonizes against hepatic lipid deposition induced by sodium arsenite in mice
10.3969/j.issn.1006-2483.2024.01.005
- VernacularTitle:伦蒂南拮抗亚砷酸钠诱导小鼠肝脏脂质沉积的实验研究
- Author:
Zongying DAI
1
;
Qianqian WU
1
;
Yuan YANG
1
Author Information
1. Guangxi Key Laboratory of Environmental Exposure Omics and Life Cycle Health , School of Public Health, Guilin Medical College , Guilin 541199, China
- Publication Type:Journal Article
- Keywords:
Sodium arsenite;
Hepatic lipid deposition;
Lentinan;
Antagonism;
Adiponectin
- From:
Journal of Public Health and Preventive Medicine
2024;35(1):20-23
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the ameliorative effect of Lentinan (LNT) on sodium arsenite (SA)-induced hepatic lipid deposition in mice. Methods C57BL/6 mice were used as the experimental subjects, which were divided into control group, SA-exposed group, LNT + SA-exposed group and LNT control group. Blood and liver tissue samples were collected at the end of the experiment, and serum glutathione transaminase (ALT) and glutathione aminotransferase (AST) levels were detected by enzyme-linked immunosorbent assay (ELISA). A part of liver tissues was stained with hematoxylin-eosin (HE) or oil red O to observe the characteristics of liver pathological damage and lipid deposition, and another part of liver tissues was used to detect triglyceride (TG) and Adiponectin (APN) levels by ELISA. Results Compared with control group or LNT control group, SA-exposed group showed the increased levels of AST and ALT, showing the characteristics of liver histopathological damage and lipid deposition, and the APN level decreased while the TG level increased (P<0.05). Compared with SA-exposed group, the levels of AST and ALT decreased in LNT + SA-exposed group, showing the reduced degree of liver tissue damage and lipid deposition, and APN level upregulated while TG level downregulated (P<0.05). Conclusion Chronic SA exposure induces liver function damage, APN downregulation and lipid deposition in C57BL/6 mice, while LNT intervention leads to the significantly improvement of hepatic damage and lipid deposition, which may be related to the elevated APN level in liver.
