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目的:通过观察心脏骤停家猪心肌氨基末端激酶(JNK)、caspase-12、钙蛋白酶(calpain)mRNA水平及蛋白表达,以及超微结构的变化,探讨山莨菪碱对心肌内质网源性调亡的保护机理。方法:用随机数字表法将23只健康家猪分为干预组(n=9),对照组(n=9),假手术组(n=5)。电致颤诱发心室纤颤,持续9min后进行标准心肺复苏,干预组为复苏过程中联合使用山莨菪碱。自主循环恢复后24h取心肌组织,透射电镜下观察心肌超微结构改变,RT-PCR检测JNK、caspase-12、calpain mRNA水平及蛋白含量变化。结果:与对照组比较,干预组心肌纤维排列较规则,心肌细胞内的内质网、线粒体和细胞核损伤轻,山莨菪碱减轻心肌细胞超微结构损伤。干预组Calpain mRNA水平较对照组减少[(0.25±0.04与(0.34±0.07),P<0.05];干预组JNK、caspase-12和calpain mRNA蛋白表达介于假手术组和对照组之间,各组间差异均有统计学意义。结论:山莨菪碱可能通过抑制内质网源性细胞凋亡的信号通路,对心脏骤停后缺血再灌注心肌有保护作用。
OBJECTIVE: To investigate the effect of anisodamine on endoplasmic reticulum (ER) activity in myocardium by observing the changes of myocardial N-terminal kinase (JNK), caspase-12, calpain mRNA and protein expression, The mechanism of death protection. Methods: Twenty-three healthy domestic pigs were divided into intervention group (n = 9), control group (n = 9) and sham operation group (n = 5) by random number table method. Electrical fibrillation induced ventricular fibrillation, continuous standard cardiopulmonary resuscitation after 9min, the intervention group for the recovery process combined with anisodamine. Myocardial tissues were harvested 24 hours after spontaneous circulation recovery and ultrastructural changes of myocardium were observed under transmission electron microscope. MRNA and protein levels of JNK, caspase-12 and calpain were detected by RT-PCR. Results: Compared with the control group, the myocardial fibers in the intervention group had a regular arrangement, the endoplasmic reticulum, mitochondria and nucleus were lightly injured in myocardial cells. Anisodamine could reduce the myocardial ultrastructure damage. The level of Calpain mRNA in the intervention group was significantly lower than that in the control group [(0.25 ± 0.04 vs 0.34 ± 0.07, P <0.05). The mRNA expression of JNK, caspase-12 and calpain in the intervention group was significantly lower than that in the control group Conclusion: Anisodamine may have a protective effect on myocardial ischemia-reperfusion after cardiac arrest by inhibiting the signaling pathway of endoplasmic reticulum-derived apoptosis.