Department of Infectious Diseases, Affiliated Hospital of Zunyi Medical University, Zunyi 56300, China.
School of Nursing, Zunyi Medical University, Zunyi 56300, China.
Contrast Media Mol Imaging. 2022 May 29;2022:6572499. doi: 10.1155/2022/6572499. eCollection 2022.
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 (IRE-1), 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 ( < 0.05); compared with group B, group C showed a significant decrease in bodyweight, fat weight, ALT, TG, and hepatic steatosis ( < 0.05). Compared with group A, the expression levels of GRP78, IRE-1, CHOP, caspase-12, and Bim in liver tissue of groups B and C mice were increased. Bcl-2 decreased ( < 0.05). Compared with group B and group C after naltrexone intervention, the expression levels of GRP78, IRE-1, CHOP, caspase-12, and Bim decreased significantly, and Bcl-2 increased significantly ( < 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.
本研究旨在探讨内质网应激诱导的小鼠肝脂肪变性中，纳曲酮对脂质代谢相关蛋白表达的影响。将 30 只近交系小鼠（C57BL/6J）分为三组：A 组（正常对照组）、B 组（模型对照组）和 C 组（纳曲酮组）。A 组雄性小鼠给予常规饮食，B、C 组小鼠给予高脂饮食。通过组织学切片观察肝脂肪变性，检测小鼠肝组织（丙氨酸氨基转移酶（ALT）和甘油三酯（TC））含量（葡萄糖调节蛋白（GRP78）、内质网跨膜蛋白激酶-1（IRE-1）、C/EBP 同源蛋白（CHOP）、半胱天冬酶-12（caspase-12）、B 淋巴瘤-2（Bcl-2）和细胞死亡介质（Bim））。与 A 组相比，B、C 组体重、脂肪重量、ALT、TC 和肝脂肪变性均显著增加（ < 0.05）；与 B 组相比，C 组体重、脂肪重量、ALT、TC 和肝脂肪变性均显著降低（ < 0.05）。与 A 组相比，B、C 组小鼠肝组织中 GRP78、IRE-1、CHOP、caspase-12 和 Bim 的表达水平升高，Bcl-2 降低（ < 0.05）。与 B、C 组纳曲酮干预后相比，GRP78、IRE-1、CHOP、caspase-12 和 Bim 的表达水平显著降低，Bcl-2 表达水平显著升高（ < 0.05）。纳曲酮能有效降低体重和脂肪组织堆积，减轻肝脂肪病变，改善脂质代谢相关蛋白和内质网应激表达，减少肝内脂质合成，保护肝细胞。
