Effect and Mechanism of Danning Tablets in the Intervention of Non-Alcoholic Fatty Liver Disease Based on IRE1α/JNK Signaling Pathway
Objective To investigate the effect and mechanism of Danning Tablets on non-alcoholic fatty liver disease(NAFLD)model rats based on inositol requiring enzyme 1α/c-Jun N-terminal kinase(IRE1α/JNK)signaling pathway.Methods A total of 32 SD rats were randomly divided into the normal diet group(group A,equal volume of normal saline,n = 8)and the high-fat diet group(n = 24).The rats in the high-fat diet group were fed for 10 weeks to replicate the NAFLD model,and they were randomly divided into the model group(group B,equal volume of normal saline),polyene phosphatidylcholine group[group C,142.5 mg/(kg·d)]group and Danning Tablets group[group D,562.5 mg/(kg·d)],eight mice in each group.Mice in each group were orally administered with corresponding drugs for six weeks.The body weight and blood glucose of rats were determined.The pathological morphological changes and lipid deposition in liver tissue were observed by hematoxylin-eosin(HE)staining and oil red staining respectively.The levels of serum insulin(INS),total cholesterol(TC),triglycerides(TG),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C),free fatty acids(NEFA),alanine aminotransferase(ALT),and aspartate aminotransferase(AST)were detected.The expression levels of IRE1α,JNK1 and phosphorylated insulin receptor substrate 1(p-IRS1)protein were detected by Western blot.Results Compared with those in group B,the levels of blood glucose,TC,TG,LDL-C,NEFA,ALT,and AST in group D were significantly lower(P<0.01),while the levels of serum INS and HDL-C in group D were significantly higher(P<0.01);the degree of fat degeneration and cell swelling of rats in group D significantly reduced,and the volume and number of lipid droplet vacuoles in group D decreased;the expression levels of IRE1α,JNK1 and p-IRS1 protein significantly decreased(P<0.01).Conclusion Danning Tablets may alleviate hepatic steatosis and improve NAFLD by down-regulating the RElα/JNK signaling pathway.