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机构地区:[1]中国医学科学院肿瘤医院麻醉科,北京市100021 [2]中国医学科学院整形外科医院麻醉科,北京市100041
出 处:《实用医学杂志》2009年第13期2047-2049,共3页The Journal of Practical Medicine
摘 要:目的:探讨雷米芬太尼对大鼠肝脏缺血再灌注损伤后期细胞凋亡因子Bax和bcl-2蛋白及其mRNA表达的影响。方法:将90只雄性Wistar大鼠分为I、R、NR、N和C组。采用70%肝脏缺血再灌注损伤模型。在大鼠肝脏缺血前分别给予生理盐水(I组)、雷米芬太尼(R组和NR组)和纳络酮(NR组和N组)。测定肝脏缺血再灌注1h和12h时的血浆丙氨酸氨基转氨酶(ALT)活性、血浆肿瘤坏死因子(TNF-α)水平以及再灌注12h时肝脏组织Bax和bcl-2蛋白及其mRNA的表达情况。结果:再灌注1h后R组的ALT活性和TNF-α水平以及再灌注12h后R组的Bax和bcl-2蛋白及其mRNA表达的比值均明显低于I组和NR组(P<0.05)。结论:雷米芬太尼可减少肝脏缺血再灌注后期阶段细胞凋亡因子Bax和bcl-2蛋白及其mRNA的表达比值。纳络酮仅能阻断部分雷米芬太尼的肝保护作用。Objective To investigate the effect of remifentanil on the expressions of cellular apoptotic factors Bax and bcl-2 protein and mRNA in a rat model of hepatic ischemia-reperfusion injury. Methods Ninety male Wistar rats were randomized to group I, R, NR, N, or C. A rat model of 70% partial hepatic ischemia/reperfusion was used. Before ischemia, the rats received normal saline (group I), remifentanil(groups R and NR), or naloxone (groups N and NR). ALT activity and plasma TNF-α levels were determined 1h and 12h after reperfusion; expressions of Bax and bcl-2 protein and mRNA in the hepatic tissues were detected 12 h following reperfusion. Results ALT activity and TNF-α levels 1 h after reperfusion and expression levels of Bax and bcl-2 protein and mRNA 12 h after reperfusion were significantly lower in group R than in groups I and NR, respectively (P 〈 0.05 for all comparisons). Conclusions Remifentanil lowers the expression levels of Bax and bcl-2 protein and mRNA in the late stage of hepatic ischemia-reperfusion injury. Naloxone can only interfere part of the protective effect of remifentanil on hepatic injury.
关 键 词:再灌注损伤 雷米芬太尼 肿瘤坏死因子-α 细胞凋亡因子Bax/bcl-2
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