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  • Title: Panax notoginseng saponins preconditioning protects rat liver grafts from ischemia/reperfusion injury via an antiapoptotic pathway.
    Author: Zhang Y, Ye QF, Lu L, Xu XL, Ming YZ, Xiao JS.
    Journal: Hepatobiliary Pancreat Dis Int; 2005 May; 4(2):207-12. PubMed ID: 15908317.
    Abstract:
    BACKGROUND: Ischemia/reperfusion (I/R) injury is a major cause of primary graft dysfunction and renders an allograft more immunogenic in orthotopic liver transplantation (OLT). Panax notoginseng saponins (PNS) has been reported to exert protective effects against I/R injury to various organs. The objective of this study is to investigate whether PNS preconditioning protects rat liver grafts from I/R injury via an antiapoptotic pathway. METHODS: Male Sprague-Dawley rats were used as donors and recipients of orthotopic liver transplantation (OLT) and were divided into PNS preconditioning group(group P) and normal saline control group (group N) randomly according to whether PNS (50 mg/kg) was injected intravenously 1 hour before liver grafts harvesting, and sham group (group S). The animals were separately killed 2, 6 and 24 hours after reperfusion. Plasma samples were collected for test of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Liver tissues were collected to detect histological changes, apoptosis and the expression of TNF-alpha, Bcl-2 and Caspase-3 mRNA. RESULTS: The serum levels of ALT and AST and the apoptosis index (AI) of liver tissue in group P were lower than in group N significantly 2, 6 and 24 hours after reperfusion. Compared with group N, the expression of TNF-alpha and Caspase-3 mRNA was reduced significantly in group P 2 and 6 hours after reperfusion and the expression of Bcl-2 mRNA was enhanced significantly in group P 6 and 24 hours after reperfusion. CONCLUSIONS: PNS preconditioning protects liver grafts from I/R injury effectively in rat OLT via an antiapoptotic pathway. The antiapoptotic mechanisms of PNS may include inhibiting the expression of TNF-alpha and Caspase-3 and enhancing the expression of Bcl-2.
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