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目的:观察纳洛酮(naloxone,Nal)对大鼠缺血再灌注心肌细胞凋亡及Fas、FasL蛋白表达的影响并探讨其机制。方法:SD大鼠24只,随机分成假手术组(Sham组)、缺血再灌注组(IR组)和纳洛酮处理组(Nal组)。原位末端标记法(TUNEL)检测心肌细胞凋亡情况;蛋白免疫印迹法(Western blotting)检测Fas、FasL蛋白表达;光镜下观察心肌组织病理学的改变。结果:与Sham组相比,IR组可见大量心肌细胞凋亡,Fas、FasL蛋白表达显著增加(P<0.01)。与IR组相比,Nal组心肌细胞凋亡显著减少,Fas、FasL蛋白表达明显降低(P<0.01)。IR组见心肌组织呈大小不等的灶性坏死,Nal组心肌坏死不明显。结论:心肌缺血再灌注时Fas、FasL表达介导心肌细胞凋亡,纳洛酮通过抑制Fas、FasL蛋白的表达而减少细胞凋亡从而起到保护心肌的作用。
Objective: To observe the effect of naloxone (Nal) on the apoptosis of myocardial cells and expression of Fas and FasL in rats with ischemia-reperfusion injury and its mechanism. Methods: Twenty-four SD rats were randomly divided into Sham group, IR group and Naloxone treatment group. The apoptosis of cardiomyocytes was detected by TUNEL. The expressions of Fas and FasL proteins were detected by Western blotting. The changes of myocardial histopathology were observed under light microscope. Results: Compared with Sham group, a large number of myocardial cells were found in IR group, and Fas and FasL expressions were significantly increased (P <0.01). Compared with IR group, the apoptosis of cardiomyocytes in Nal group was significantly reduced, while the expression of Fas and FasL protein was significantly decreased (P <0.01). IR group showed myocardial tissue showed varying degrees of necrosis, necrosis in Nal group was not obvious. Conclusion: The expression of Fas and FasL during myocardial ischemia / reperfusion can induce the cardiomyocyte apoptosis. Naloxone can protect the myocardium by inhibiting the expression of Fas and FasL and decreasing the cell apoptosis.