机构地区:[1]广州军区广州总医院157附属医院药械科,510510 [2]广东省人民医院血管甲状腺腹壁疝外科
出 处:《中华实验外科杂志》2011年第7期1130-1132,共3页Chinese Journal of Experimental Surgery
摘 要:目的探讨前列地尔对兔肝脏缺血再灌注损伤时,有效减少肝细胞凋亡的机制。方法将健康新西兰兔36只随机分为3组:对照组、缺血再灌注组和前列地尔组,3组分别在再灌注60min和90min时,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)水平。取肝中叶检测兔诱导型一氧化氮合酶(iNOS)、髓过氧化物酶(MPO)以及bcl-2、bax和Caspase-3蛋白表达;并用原位缺口末端标记法(TUNEL)染色比较各组肝细胞凋亡。结果与对照组比较,缺血再灌注组和前列地尔组在再灌注后ALT、AST、LDH水平均大幅上升(P〈0.05);但前列地尔组兔在再灌注60、90min时ALT、AST、LDH水平明显低于缺血再灌注组(P〈0.05);与对照组比较,缺血再灌注组肝细胞bcl-2、bax、Caspase-3的表达明显增强;前列地尔组与缺血再灌注组比较表达均减弱,但仍强于对照组。TUNEL法显示前列地尔组、缺血再灌注组与对照组比较凋亡细胞数增多,前列地尔组与缺血再灌注组比较凋亡细胞数减少;与对照组比较,缺血再灌注组与前列地尔组iNOS与MPO的活性明显增强,前列地尔组与缺血再灌注组比较,该两者活性明显减弱。结论前列地尔在肝脏缺血再灌注损伤时能有效地保护肝功能,减少肝细胞的损伤,其作用机制可能是通过减少细胞脂质过氧化,从而降低bcl-2、bax、Caspase-3等凋亡基因的表达。Objective To study the protective the positive effects of alprostadil Hepatocyte Apoptosis by Liver Ischemia-Reperfusion Injury in rabbits. Methods Thirty-six rabbits were made the model of liver ischemia-reperfusion injury, and randourly divided into three groups:Control group, Ischemia-Reper- fusion Injury group and Alprostadil intervention group. The alanine aminotransferase (ALT) , aspartate aminotransferase (AST) , lactate dehydrogenase (LDH) were determined; Each group inducible nitric oxide synthase (iNOS) , myeloperoxidase (MPO) and bcl-2, bax, Caspase-3 and apoptosis of the hepatocyte by TUNEL were assayed at 60 and 90 min after reperfusion. Results The ALT, AST, LDH concentration in plasma in Ischemia-Reperfusion Injury group and Alprostadil intervention group were increased obviously at 60, 90 min after reperfusion and it was significantly higher than that in the Control group in the same time point (P 〈 0. 05). And the ALT, AST, LDH concentration in plasma in Alprostadil intervention group was significantly lower than that in the in Ischemia-Reperfusion Injury group in the same time point (P 〈 0.05). The level of bcl-2, bax, Caspase-3 in the liver tissue in the Control group was smaller, but the obvious increase of the expression those was found in the Ischemia-Reperfusion Injury group and Alprostadil intervention group. Compared with those in the lschemia-Reperfusion Injury group group, the expression of bcl-2, bax, Caspase-3 in the Alprostadil intervention group werw obviously smaller ( P 〈 0.05 ). The contents of iNOS and MPO in liver tissue in the Ischemia-Reperfusion Injury group and Alprostadil intervention group were significantly higher than that in the Control group ( P 〈 0. 05 ). Conclusion Alprostadil could be used to protect liver ischemia-reperfusion injury, it could decrease oxygen free radicals generation, inhibit neutrophils aggregating and activating in the liver, thereby inhibiting expression of bcl-2, bax, Caspase-3.
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