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目的:研究芍药苷(Paeoniflorin)预处理对大鼠心肌缺血再灌注损伤(MIRI)的保护性作用并对其可能机制进行探讨。方法 :制备大鼠心肌缺血再灌注损伤模型,随机分为模型组、假手术组、芍药苷60mg/kg组、30mg/kg组(n=20);取心脏测定心肌梗死面积,HE染色观察组织细胞结构,免疫组化检测心肌组织中NF-κB和ICAM-1的表达;取血测定血清中LDH、AST、CK和CK-MB含量。结果:与模型组比较,芍药苷60mg/kg组和30mg/kg组心肌梗死面积均明显降低;HE染色切片提示各给药组心肌细胞损伤较模型组为轻,且具有浓度相关性;芍药苷60mg/kg组、30mg/kg组NF-κB、ICAM-1的表达明显降低;芍药苷60mg/kg组血清CK含量降低,同时该组CK-MB亦降低显著。结论:芍药苷预处理对大鼠MIRI具有保护性作用,其机制与抑制细胞膜脂质过氧化,以及通过抑制NF-κB蛋白表达进而影响受NF-κB调控的下游炎性反应途径有关。
Objective: To study the protective effect of Paeoniflorin preconditioning on myocardial ischemia-reperfusion injury (MIRI) in rats and its possible mechanism. Methods: The model of myocardial ischemia-reperfusion injury in rats was prepared and randomly divided into model group, sham operation group, paeoniflorin 60mg / kg group and 30mg / kg group (n = 20) Tissue cell structure and expression of NF-κB and ICAM-1 in myocardial tissue were detected by immunohistochemistry. Serum levels of LDH, AST, CK and CK-MB were determined by blood sampling. Results: Compared with the model group, the area of myocardial infarction of paeoniflorin 60mg / kg group and 30mg / kg group were significantly reduced; HE staining showed that the myocardial cell injury of each administration group was lighter than the model group and had a concentration-related relationship; Paeoniflorin The expression of NF-κB and ICAM-1 in 60mg / kg group and 30mg / kg group decreased obviously. The content of serum CK in paeoniflorin 60mg / kg group decreased and the CK-MB of the group also decreased significantly. CONCLUSION: Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to the inhibition of cell membrane lipid peroxidation and the downstream inflammatory response regulated by NF-κB by inhibiting NF-κB protein expression.