| Background: Hepatic ischemia reperfusion (HIR) injury is a common acute disease of surgery. Organ injury is a serious complication of HIR. Acute liver injury(ALI) usually occurs early in organ injury after HIR. At present, it can induce endotoxemia transposal. Endotoxemia can gather in liver and lung and nephridium continually. Liver is the most important and early organ. It is deemed to be a one of major reason for ALI after HIR.OLT is the most important progress in the treatment of end-stage liver disease. The shortage of the donor liver significantly increased with the growing number of the patients waiting for OLT. In USA and other westen countries, the donor livers were got without HIR problem, but the donor livers were got from NHBD (non-heart-beating donor) in China which unavoidablly experienced HIR. Apart from the factors as surgical technics and expenses, the quality of the donor liver plays an important role in the restrict of efficacy of OLT in our country. Recently, research shows HIR is an dynamic course related to the time, degree and reperfusion while going with HIR. HIR may be the one ofmain cause of the primary graft non-function after OLT. So, it has great clinic significance to deeply go into the research,, on the mechanism of the ALI after HIR and the prevention way.I kappa B kinase(IKK) -|3 plays a crucial role in the activatory process of nuclear factor -kappa B (NF-icB) which is an ubiquitous rapid response transcription factor, it can degrade inhibitor-kappa B (I-B), expose the nuclear localization sequence (NLS), and make NF-B translocate from the cytoplasm to the nucleus where it upregulates the transcription of inflammatory cytokines that lead to uncontrollable inflammatory reaction and induce ALI. PDTC is one of antioxidant. It has many biological effects, including protective effect of cells and anti-inflammatory action.This study was conducted to establish the experimental animal models of ALI by HIR and endotoxin(ET), to evaluate the expression of IKK-pmRNA and activation of NF-icB activation in liver tissues and the expression of tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6) in liver tissuses and to discuss the role of IKK-NF-B pathway in pathogenesis of ALI after HIR; At the same time, by treatment with PDTC we observed its protective effects on ALI and investigate its role in molecular mechanisms of anti-inflammatory action. We intended to approve that intervening IKK- NF-KB pathway was an effective approach to preventing the generation and development of ALI after HIR and to provide experimental basis for the prophylaxis and treatment of ALI after HIR.Methods Wister rats were divided randomly into sham control group(A group), HIRE group(B group), and PDTC treatment group(C group). In B group, hepatic reperfusion was given after 60 minutes of ischemia by interruption of the arterial and portal venous bloodsupply to the left lobes and middle lobes of the liver and LPS (2.5 mg kg-1) was injected via the dorsum vein of penis. In C group, PDTC(120 mg kg-1) were injected via the dorsum vein of penis before ischemia reperfusion. In A group, midline laparotomy was performed without vascular occlusion and treatment. Expression levels of IKK were measured with In situ hybridization(ISH). The NF-B activities were determined with EMSA. Expression levels of TNF-a and IL-6 were measured with immunohistochemistry (IH). Serum levels of ALT were measured.Results (1) Expression level of IKK was increased markedly from 0 to 12h and peaked 3h after.reperfusion in B group. Expression level of IKK was lowered markedly in C group from 0 to 12h after reperfusion as compared with B group (P<0.05) . (2) NF-KB was activated 0-12h after reperfusion and activities of NF-icB were maximal 3h after reperfusion in B group rats as compared with A group (P<0.01) . NF-icB activities were significantly lower in C group than in B group from 0 to 12h after reperfusion (P<0.05) . (3) Expression level of TNF-a and IL-6 was increased markedly from 0 to 12h and peaked 6h after repe...
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