Study Of Salidroside Protective Effects On Rats With Sever Acute Pancreatitis

Objective To study the salidroside protective effects on rats with severe acute pancreatitis and the possible mechanism of it.Methods Fifty healthy male Wistar rats were randomly divided into sham operation group(Sham group),severe pancreatitis group(SAP group),15mg/kg dose of salidroside treatment group(Sal 15 group),30mg/kg dose of salidroside treatment group(Sal 30 group)and 60mg/kg dose of salidroside treatment group(Sal 60 group),and then there were ten rats in each group.Sham group was injected retrograde normal saline into pancreatic duct,while the five percent sodium taurocholate was injected retrograde into pancreatic duct to establish severe acute pancreatitis model in SAP group and every Sal group.After successful modeling,different doses of salidroside was intraperitoneally injected in each Sal group twice every six hours.Blood samples and pancreatic tissues were collected at twenty-four hours after modeling in the five groups.The AMY activity and TNF-? level were detected by ELISA kit,the way of Western blot was used to check the expression of LC3,mTOR and NF-? B protein in pancreatic tissue.The histopathological changes of pancreas were observed under the light microscope.Results(1)The AMY activity in SAP and all the Sal groups was significantly higher than that in Sham group(P<0.05);All the Sal groups of which was significantly lower than that in SAP group(P<0.05),and the most significant decrease was in Sal 60 group.There was significant difference of AMY activity among all the Sal groups(P<0.05).(2)The level of TNF-? in SAP and all the Sal groups was significantly higher than that in Sham group(P<0.05);Which in Sal 30 group and Sal 60 group was significantly lower than that in SAP group(P<0.05),and the most significant decrease was in Sal 60 group;There was significant difference of TNF-? level among all the Sal groups(P<0.05).(3)The relative expression level of LC3 II in SAP group and all the Sal groups was significantly down-regulated compared with the Sham group(P<0.05),Which in Sal30 group and Sal 60 group was significantly up-regulated compared with the SAP group after salidroside for treatment(P<0.05),and the most significant increase was in Sal 60 group;And there were statistically significant differences of LC3 II expression among all the Sal groups(P<0.05).(4)The relative expression level of p-mTOR in SAP group and all the Sal groups was significantly up-regulated compared with the Sham group(P<0.05),Which in Sal 30 group and Sal 60 group was significantly down-regulated compared with the SAP group after salidroside for treatment(P<0.05),and also the most significant increase was in Sal 60 group;And there were statistically significant differences of p-mTOR expression among all the Sal groups(P<0.05).(5)Compared with Sham group,the p-p65 relative expression level in SAP group and all the Sal groups was significantly up-regulated(P<0.05),Which in Sal 30 group and Sal 60 group was lower than that in SAP group after salidroside for treatment(P<0.05),and the most obvious decrease was in Sal 60 group;And there were statistically significant differences of p-p65 expression among all the Sal groups(P<0.05).(6)The histopathological changes of the pancreas were as follows: the degree of pathological damage of pancreatic tissues in SAP group and all the Sal groups was significantly worse than that in Sham group,while which in all the Sal groups was reduced compared with the SAP group after treatment of the salidroside and the most significant reduction was in Sal 60 group.Conclusions Salidroside not only significantly reduced the AMY activity in serum,TNF-?level in plasma and the p-p65 relative expression in pancreatic tissue to decreased the pathological damage of pancreas,but also significantly inhibited the relative expression of p-mTOR and up-regulated the autophagy activity of pancreatic cells.The mechanism of which may be that salidroside plays a protective role in the pancreas by inhibiting the NF-?B—TNF-? inflammatory pathway and(or)the mTOR-autophagy pathway.