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生黄合剂对缺血再灌注模型大鼠心肌细胞凋亡及相关基因bax、bcl-2 mRNA的影响 被引量:9

Influence of Sheng-Huang mixture on cardiocyte apoptosis and bax and bcl-2 mRNA expression in a rat model of ischemia-reperfusion injury
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摘要 背景:生黄合剂由中药生脉饮和黄芩茎叶总黄酮组成,已有研究表明其通过抗炎、调节免疫功能等对心肌缺血有保护作用,但对缺血再灌注损伤后心肌细胞凋亡的作用机制尚未阐明。目的:探讨生黄合剂对缺血再灌注模型大鼠心肌细胞凋亡及相关基因bcl-2、bax mRNA表达的影响。方法:将36只SD大鼠随机分为6组,即生黄合剂低、中、高剂量组、阳性药物对照组、空白组、模型组,每组6只,分别给药7 d后,建立心肌缺血再灌注损伤模型。用TUNEL法检测心肌细胞凋亡情况,RT-PCR法检测缺血再灌注区心肌bax、bcl-2 mRNA的表达。结果与结论:(1)与模型组比较,生黄合剂治疗组bcl-2 mRNA表达显著升高(P<0.05),bax mRNA表达显著降低(P<0.05),使bcl-2/bax比值升高,心肌细胞凋亡指数明显降低(P<0.05);(2)结果证实,生黄合剂对大鼠心肌组织缺血再灌注有保护作用,其机制可能是通过上调bcl-2 mRNA的表达、下调bax mRNA的表达,提高bcl-2/bax比值,从而起到抑制心肌细胞凋亡。 BACKGROUND: Sheng-Huang mixture including Chinese medicine Shengmai Decoction and total flavonoids of stems and leaves of radix has been shown to resist inflammation, regulate immune function, and protect ischemic myocardial tissues. However, its effect on the apoptosis of cardiac muscle cells after ischemia/reperfusion injury remains unclear. OBJECTIVE: To investigate the effects of Sheng-Huang mixture on cardiocyte apoptosis and bax and bcl-2 mRNA expression in rats with ischemia-reperfusion injury. METHODS: Thirty-six Sprague-Dawley rats were divided randomly into six groups: low-dose, moderate-dose and high-dose Sheng-Huang mixture, positive control, blank and model groups(n=6). After 7 days of administration, models of myocardial ischemia-reperfusion injury were established. TUNEL was used to detect myocardial apoptosis. RT-PCR was utilized to measure bax and bcl-2 mRNA expression in the ischemic and reperfusion region. RESULTS AND CONCLUSION:(1) The bcl-2 mRNA expression was significantly higher in the Sheng-Huang mixture group than in the model group(P〈0.05), but bax mRNA expression was significantly lower(P〈0.05). Thus, bcl-2/bax ratio increased. In addition, apoptosis index was more significantly decreased in the Sheng-Huang mixture group(P〈0.05).(2) Results demonstrated that Sheng-Huang mixture can protect rat myocardium against ischemia/reperfusion injury, and effectively increase the bcl-2/bax ratio and inhibit the apoptosis of cardiomyocytes, and the underlying mechanism is mediated by up-regulating bcl-2 mRNA expression and down-regulating bax mRNA expression.
机构地区 承德医学院
出处 《中国组织工程研究》 CAS 北大核心 2016年第27期4049-4054,共6页 Chinese Journal of Tissue Engineering Research
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参考文献36

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