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目的观察急性甲基苯丙胺(METH)对中毒大鼠心肌细胞L型钙通道(LTCCs)α1c、β2亚基蛋白的表达,探讨METH中毒的心肌毒性机制。方法采用腹腔注射盐酸甲基苯丙胺生理盐水溶液的方法,建立急性METH中毒模型。取大鼠心肌组织,采用HE和免疫组化方法进行染色,观察心肌形态学变化,对α1c、β2亚基免疫组化染色进行半定量分析检测,并比较实验组和对照组大鼠心肌染色和半定量分析结果的差异。结果急性METH中毒大鼠心肌经HE染色,可见心肌细胞水肿、断裂、嗜酸性增强,心肌细胞肌溶灶形成,或可见心肌收缩带坏死、心肌间质出血和心肌间质纤维增生;免疫组化染色可见α1c、β2亚基明显的阳性表达,其半定量结果与对照组有显著差异性(P<0.01)。结论急性METH中毒对大鼠心肌重要的离子通道LTCCs有影响,其两个重要亚基蛋白α1c和β2在中毒后均有明显升高,推测可能通过影响LTCCs的表达,导致心律失常及心室肌细胞损伤。
Objective To investigate the expression of α1c and β2 subunit proteins in L-type calcium channels (LTCCs) induced by acute methamphetamine (METH) in rats and explore the mechanism of myocardial toxicity induced by METH poisoning. Methods Acute METH poisoning model was established by intraperitoneal injection of methamphetamine hydrochloride saline solution. The myocardial tissue of rats was taken and stained with HE and immunohistochemistry method to observe the morphological changes of myocardium. Semi-quantitative analysis of α1c and β2 subunit immunohistochemical staining was performed. The myocardial staining and Semi-quantitative analysis of the differences. Results The myocardium of acute METH poisoning rats were stained by HE. The edema, rupture and eosinophilia of cardiomyocytes were observed, and the formation of myofibrillar cells in cardiomyocytes, necrosis of myocardial contractile band, myocardial interstitial hemorrhage and myocardial interstitial fibrosis were observed. Immunohistochemistry The results showed that the expression of α1c and β2 subunits were significantly higher than that of the control group (P <0.01). Conclusions Acute METH poisoning may affect the LTCCs of important ion channels in rat myocardium. The two major subunit proteins α1c and β2 are significantly increased after poisoning. It is speculated that acute METH poisoning may affect the expression of LTCCs and cause arrhythmia and ventricular myocytes damage.