The Effect And Significance Of COX-2 Inhibitors In The Expression Of Atg7 And LC3?/LC3?of Non-alcoholic Fatty Hepatocytes

Objective: To investigate the effect of cox-2 inhibitors in the expression of Atg7 and LC3?/LC3?of nonalcoholic fatty hepatocytes, and what significance does it mean?Methods: Randomly divided 36 SD rats into normal control group, NAFLD model group, nimesulide treatment group, 12 rats each.All of the rats were fed 7 days to adapt the environment, Samples in all groups except those in the normal control group were reared with high fat diet for 12 weeks, and indexes of hepatic fibrosis were observed. Normal food for 12 weeks to normal control group. Nimesulide treatment group rats were given by gavage once a day with 6mg/kg from the 1st day at the beginning of the modeling with high- fat diet simultaneously. The animals fasted overnight and sacrificed at 12 weeks.To draw blood from inferior vena cava of each rat, blood serum was separated to analyse cholesterol(TC), triglycerides(TG) with the automatic biochemical analyzer. Liver pathology by electron microscope observation with oil redstaining, hematoxylin and eosin staining. Western Blot applied in the detection of the expression of Atg7 and LC3?/LC3?in rat liver tissues.Results:1.Serum levels of TC and TG in NAFLD model group, and in nimesulide treatment group were increased significantly compared to the control group(P<0.05); The serum levels of TC and TG in nimesulide treatment group were markedly decreased compared to the NAFLD model group(P<0.05).2.On the basis of oil red staining, hematoxylin-eosin(HE) staining, the NAFLD model group have significantly steatotic(P<0.05), while in the nimesulide treatment group steatotic area is decreased significantly compared with NAFLD model group(P<0.05).3.The testing results of Western Blot indicate that:the expression levels of Atg7 and LC3?/LC3?in liver tissue of rats were significantly increased than NAFLD model group(P<0.05).Conclusions:Cox-2 inhibitors can raise the expression of Atg7 and LC3?/LC3?in the nonalcoholic fatty hepatocytes, and then promotes the autophagy of nonalcoholic fatty liver disease.