莫诺苷对大鼠心肌缺血再灌注损伤的保护作用及可能机制

目的 通过观察莫诺苷对大鼠缺血再灌注损伤(MIRI)心肌组织中凋亡相关基因Bcl-2和Bax表达及心肌梗死面积百分比、心肌组织形态、心肌酶谱的影响,探讨莫诺苷是否可以发挥心肌保护作用并研究可能的相关机制。 方法 健康雄性SD大鼠,随机分为假手术组、缺血再灌注组、莫诺苷90 mg/(kg·d)]组。以左冠状动脉前降支穿线结扎法制备SD大鼠心肌缺血模型,30 min后放松结扎线制备再灌注模型。分别测定各组大鼠血清肌酸激酶同工酶(CK-MB)水平、左心室心肌梗死面积百分比、制备心肌组织切片及采用PCR技术测定Bcl-2和Bax基因的表达情况。 结果 与假手术组相比,缺血再灌注组和莫诺苷组大鼠血清CK-MB值显著增高(P<0.01)、心肌梗死面积百分比显著增高(P<0.01)、组织结构病理损伤加剧、Bcl-2、Bax表达增强(P<0.01)。与缺血再灌注组相比,莫诺苷组大鼠CK-MB值显著下降(P<0.01),梗死面积百分比显著减小(P<0.05),组织病理损伤减轻及Bax表达降低(P<0.05),Bcl-2表达增高(P<0.01)。 结论 莫诺苷对大鼠心肌缺血再灌注损伤有保护作用,其作用机制可能与莫诺苷通过上调缺血再灌注心肌组织中Bcl-2基因、下调Bax基因表达而抑制细胞凋亡有关。 

The protection and related mechanism of morroniside in rat model of myocardial ischemic reperfusion injury

Objective To investigate the effect of morroniside on myocardial ischemia reperfusion injury (MIRI) in a rat model of myocardial ischemic reperfusion injury and reveal the possible mechanisms behind it. The obvervational index mainly include the expression of the apoptosis gene Bcl-2 and Bax, the infarction area percentage, the tissue section and the myocardial enzyme. Methods Healthy male Sprague Dawley rats were randomly allocated to three groups:sham, ischemia/reperfusion (IR) and morroniside. The group of IR and morroniside are made ischemia reperfusion injury (IRI) models through surgery. Serum creatine kinase isoenzyme (CK-MB) were assayed. The infarct size was determined by triphenyl tetrazolium chloride staining. The tissue section are observed through microscope. The apoptosis gene Bax and Bcl-2 was assessed through real-time polymerase chain reaction. Results Compared with the sham group, the infarct size percentage, the serum creatine kinase isoenzyme (CK-MB) level, the damage of tissue and the Bax and Bcl-2 gene expression level were significantly raised in the IRI and morroniside group. Compared with the IR group, the infarct size percentage, the serum creatine kinase isoenzyme (CK-MB) level, the damage of tissue and the Bax gene expression level were significantly reduced in the morroniside group, while Bcl-2 gene expression level was significantly increased. Conclusion This experiment demonstrate that morroniside provides an enhanced protection against myocardial IRI and may through the Bcl-2-linked apoptotic signaling pathway.