Expression of hepatic Connexin43 in young mouse model of nonalcoholic fatty liver disease
Objective To explore the change of Connexin43(Cx43)expression in the liver of young mouse model of nonalcoholic fatty liver disease(NAFLD),and to analyze its relationship with hepatocyte lipid deposition,endoplasmic reticulum stress,inflammatory infiltration and oxidative stress,in order to lay a foundation for further exploration of possible intervention targets.Methods A total of 24 4-week-old C57BL/6J mice were selected in to this study,and were randomly divided into two groups fed with normal diet and high-fat diet for 13 weeks,respectively.Then normal control and NAFLD model were established.The body weight and liver weight of mice were measured.Blood and liver samples were collected to detect blood glucose,blood lipids,cholesterol and triglycerides.The degree of liver lesion was observed by HE and oil red O staining.Immunohistochemical staining was used to detect the expression and localization of Cx43 in mouse liver tissue,and its correlation with lipid deposition related index CD36,inflammatory infiltration and oxidative stress related index CD68,F4/80 and endoplasmic reticulum stress related index GRP78,pIRE1 expression.Results Compared with the normal control group,the body weight,liver weight,triglyceride,cholesterol and blood glucose levels in NAFLD group were significantly higher(P<0.001).At the same time,it was found that compared with the control group,the expression of Cx43 in the liver of NAFLD mice was significantly up-regulated,and the expression of GRP78,IRE1,CD68,F4/80 and CD36 was also up-regulated(P<0.01).Correlation analysis showed that the expression of Cx43 was positively correlated with the expression levels of CD36(r=0.724),CD68(r=0.544),F4/80(r=0.648),F4/80(r=0.575)and IRE1(r=0.658).Conclusion Hepatic Cx43 expression is up-regulated in the young mouse model of NAFLD,which may be involved in the regulation of the pathological changes of lipid deposition,endoplasmic reticulum stress,inflammatory infiltration and oxidative stress in fatty liver.