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作 者:张少波[1] 何谦[1] 葛亮[1] 施建设[1] 王耿杰[1] 张诚华[1]
机构地区:[1]解放军第180医院普外科,福建泉州362000
出 处:《临床军医杂志》2011年第4期608-610,共3页Clinical Journal of Medical Officers
摘 要:目的探讨重组人促红细胞生成素(rhEPO)对核因子(NF)-κB活化的影响在肝缺血再灌注(I/R)损伤中的作用。方法制作大鼠部分肝I/R模型,分为:假手术组(A组),肝缺血90 min组(B组),肝缺血90 min,再灌注120 min组(C组),肝缺血90 min,再灌注120min,加重组人促红细胞生成素(建模前1、3 d及5 d给予rhEPO100 U/kg)组(D组)。光镜观察肝脏组织学改变,测定血清肝酶学水平,用Western blot技术检测肝组织中核转录因子-κB(NF-κB)p65表达,用双抗体夹心酶联免疫吸附法测定血清中肿瘤坏死因子-α(TNF-α)表达水平。结果A组肝细胞索排列有序,肝细胞形态正常;B组肝小叶结构紊乱,肝血窦和中央静脉有轻度淤血,内皮细胞和肝细胞水肿变性;C组肝细胞坏死较明显,D组上述改变明显减轻。和C组相比,D组血清肝酶学指标、NF-κB p65和TNF-α的表达水平明显下降,且差异均有统计学意义(P<0.05)。结论 重组人促红细胞生成素能抑制肝脏NF-κB的活化,对肝脏缺血再灌注损伤具有保护作用。Objective To investigate the effect of recombinant human erythropoietin(rhEPO) in preventing ischemic reperfusion injury by NF-κB after hepatic ischemia reperfusion injury.Methods Models of rats with hepatic ischemia reperfusion were established and 4 groups(n=8 in each group) were set up: group A as normal control group;group B as lobar hepatic ischemia 90 min;group C as hepatic ischemia 90 min followed by reperfusion 120 min;and group D as hepatic ischemia reperfusion with rhEPO treatment(rhEPO 100U/kg subcutaneous injection at 1d,3d and 5d before modeling).In addition to histological examination of the liver,the nuclear factor-κB(NF-κB) p65 relative level of tissue was detected by Western blot analysis and the TNF-α level of blood was detected by ABC enzyme linked immunosorbent assay.Results The hepatic cell cords arranged orderly and hepatocyte morphology was normal in group A.Structural disorder of hepatic lobules,mild congestion in hepatic sinusoid and central vein,hydropic degeneration of endothelial cell and hepatocyte occurred in group B.Hepatocyte necrosis was obvious in group C.The changes of above indexes were significantly lighter in group D.The expression level of serum NF-κB p65,TNF-α and liver enzymology index of serum in the group D were lower than the group C,and the difference has statistical significance(P0.05).Conclusion The rhEPO could markedly reduce the activity of NF-κB in liver tissue and could prevent ischemia reperfusion injury of liver.
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