Effects of Naltrexone on Expression of Lipid Metabolism-Related Proteins in Liver Steatosis Induced by Endoplasmic Reticulum Stress in Mice.

This study aimed to explore the effect of naltrexone on the expression of lipid metabolism-related proteins in liver steatosis induced by endoplasmic reticulum stress in mice. Thirty inbred mice (C57BL/6J) were divided into three groups: group A (normal control group), group B (model control), and group C (naltrexone group). The male mice in group A were fed a regular diet, and the mice in groups B and C were fed a high-fat diet. Liver steatosis was observed by histopathological sections. Mouse liver (alanine aminotransferase (ALT) and triglyceride (TC)) content (glucose regulatory protein (GRP78), endoplasmic reticulum transmembrane protein kinase-1 α (IRE-1 α ), C/EBP source protein (CHOP), cysteine-containing aspartate proteolytic enzyme 12 (caspase-12), B lymphoma-2 (Bcl-2), and cell death mediator (Bim)) was detected. Compared with group A, bodyweight, fat weight, ALT, TG, and hepatic steatosis were significantly increased in B and C groups ( P < 0.05); compared with group B, group C showed a significant decrease in bodyweight, fat weight, ALT, TG, and hepatic steatosis ( P < 0.05). Compared with group A, the expression levels of GRP78, IRE-1 α , CHOP, caspase-12, and Bim in liver tissue of groups B and C mice were increased. Bcl-2 decreased ( P < 0.05). Compared with group B and group C after naltrexone intervention, the expression levels of GRP78, IRE-1 α , CHOP, caspase-12, and Bim decreased significantly, and Bcl-2 increased significantly ( P < 0.05). Naltrexone can effectively reduce bodyweight and adipose tissue accumulation, reduce liver fat lesions, improve the expression of lipid metabolism-related proteins and endoplasmic reticulum stress, reduce liver lipid synthesis, and protect liver cells.