Objective:To study the expression and significance of HMGB1in the acute pancreatitis of LC3â…¡ activated autophagy signal for producing a new theoretical foundation to the development of acute pancreatits about the clinical treatment and the mechanism.Method:48SD male rats were randomly divided into sham-operated (SO) group, and the experimental (ANP) group which were injected with5%sodium taurocholate into the bili-pancreatic duct retrogradely to produce acute pancreatitis rat models.The SO grape were injected with normal saline in equal quantity.Experimental group (ANP group) rats were sacrificed at0h(n=4),3h (n=8),6h (n=8),12h (n=8), and24h (n=8) after modeling, and the sham-operated group (SO group) rats were sacrificed at3h(n=4),6h(n=4),12h(n=4),24h(n=:4)time points to the experimental group. The contents of amylase was detectived by Elisa assay,and the pathological of pancreas tissues were made histological score by HE staining. The development of autophagic vacuole in acute panreatitis pancreatic acinar cell at different time points was observed by transmission electron microscope(TEM);Meantime,HMGB1and LC3â…¡ were detected by western blot in acute pancreatitis tissue at different time intervals.Results:The acute necrosis pancreatitis modes were made successful y.In the acute pancreatitis, HMGB1did not change significance at0hã€3h and6h(P>0.05). However,HMGB1levels in pancreatic tissue increased remarkably at the12th hour, and maintained up to24h post-acute pancreatitis (P>0.05). LC3II levels in pancreatic tissue increased constantly with the development of the actue pancreatitits(P<0.05).Conclusion:1.HMGB1was different from some early inflammation factors,which increased obviously in the pancrea tissues at the late of the acute pancreatitis.2.HMGB1may be in favor of maintaining the expression of the LC3II in the acute pancreatitis,aggravating the development of the acute pancreatitis. |