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The Liver Injury Mechamisms In Rats With Sever Acute Pancreatitis And Protective Effects Of N-acetylcysteine Homocysteine To Liver

Posted on:2012-01-28Degree:MasterType:Thesis
Country:ChinaCandidate:W LiFull Text:PDF
GTID:2234330374979555Subject:Surgery
Abstract/Summary:PDF Full Text Request
Objective:To explore liver injury key mechanisms in rats with severe acutepancreatitis (SAP) and protective effects and mechanisms of N-acetylcysteine to liverinjury of rats with severe acute pancreatitis.Methods:Ninety SD rats were randomly divided into group A (sham operationgroup), group B (SAP group) and group C (therapeutic group with N-acetylcysteine)each group of30only.SAP was inflicted with5%sodium tauroeholate to groupe Band C by the method of retrograde pancreatic injection.In group C rats recieived oneintravenous injection of NAC(200mg/kg)lh after taurocholate injection.A1l theanimals were sacririced randomly in4h、8h、12h after induction ofpanceatitis.Immediately from the right ventricle picks line in serum amylase, liverfunction (AST, ALT) and MDA in check,Take liver and pancreatic tissue br dye withhematoxyli-eosin,and do the pathological examination. SP immunohistochemicalmethod to detect the liver tissue the nf-kappa B activity; Intrahepatic expression ofTNF-αMrna was assayed by RT-PCR.Result: B model group after the NF-κB was significantly increased,TNF-αmRNA over-expression in liver tissue and serum MDA increased.B group atdifferent time points significantly higher than the A group(P<0.01),C group wassignificantly lower than the B group (P<0.01),C group amylase,AST,ALT and MDAlevels compared with the B group significantly decreased(P<0.01).Conclusions:Liver tissue the nf-kappa B activation and TNF alpha mRNAexpressions are a SAP intercurrent liver injury is one of the mechanism,NAC byinhibiting liver the nf-kappa B activity, and rein in TNF alpha mRNA expressions, toSAP liver damage has certain protective effect.
Keywords/Search Tags:severe acute pancreatitis(SAP), liver injury, N-acetylcysteine
PDF Full Text Request
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