基于细胞凋亡探讨白金方对心肌缺血再灌注损伤大鼠的心肌保护作用及机制

Exploring the Cardioprotective Effects and Mechanism of Baijin Formula on Myocardial Ischemia/Reperfusion Injury in Rats Based on Apoptosis Pathway

目的:通过构建心肌缺血再灌注损伤(MIRI)大鼠模型,基于细胞凋亡相关通路,观察白金方(乌腺金丝桃、薤白、瓜蒌)对细胞凋亡的影响,进而探讨其对大鼠心肌缺血再灌注损伤的心肌保护作用及相关机制。方法:将3月龄的SD大鼠随机分为空白组、假手术组、模型组、预处理组、白金方不同比例配伍组(乌腺金丝桃:薤白:瓜蒌)1:1:3组、2:1:3组、3:1:3组。构建大鼠MIRI模型。白金方不同比例配伍组使用不同比例配伍的白金方,灌胃14 d,其余组给予生理盐水灌胃14 d。采用ELISA法测定各组大鼠心肌组织中MDA、SOD含量;使用荧光定量PCR检测心肌细胞凋亡相关基因(BCL-xl、BCL-2)表达水平。结果:白金方(乌腺金丝桃:薤白:瓜蒌)1:1:3组、2:1:3组、3:1:3组均能使心肌组织中的氧化应激指标MDA、SOD含量降低(P<0.05)。2:1:3组、3:1:3组不同程度增加抑制凋亡基因BCL-xl、BCL-2 mRNA的表达水平(P<0.05),进而抑制细胞凋亡,其中3:1:3组抗凋亡能力最佳(P<0.01)。结论:白金方对大鼠MIRI过程的凋亡、抗凋亡基因表达水平进行调控,发挥其心肌保护作用。

Objective:To investigate the cardioprotective effects and mechanisms of Baijin Formula(composed of Hypericum japonicum,Allium macrostemon,and Trichosanthes kirilowii)on myocardial ischemia/reperfusion injury(MIRI)in rats through apoptosis-related pathways.Methods:A rat model of MIRI was constructed,and 3-month-old SD rats were randomly divided into the blank group,sham operation group,model group,pretreatment group,and different ratio groups of Baijin Formula(Hypericum japonicum:Allium macrostemon:Trichosanthes kirilowii in ratios of 1:1:3,2:1:3,and 3:1:3).The Baijin Formula groups were administered the formula at different ratios for 14 days by gavage.The contents of malondialdehyde(MDA)and superoxide dismutase(SOD)in myocardial tissue were measured by ELISA.The expression levels of apoptosis-related genes(BCL-xl and BCL-2)were detected using quantitative PCR to understand the myocardial protective effects of Baijin Formula on MIRI rats.Results:The Baijin Formula groups(1:1:3,2:1:3,3:1:3)significantly reduced the oxidative stress markers MDA and SOD in myocardial tissue(P<0.05).The 2:1:3 and 3:1:3 groups significantly increased the expression levels of anti-apoptotic genes BCL-xl and BCL-2 mRNA(P<0.05),thereby inhibiting apoptosis,with the 3:1:3 group showing the strongest anti-apoptotic effect(P<0.01).Conclusion:Baijin Formula exerts cardioprotective effects in the process of MIRI by regulating apoptosis and the expression levels of anti-apoptotic genes.