红景天对大鼠心肌缺血损伤的保护作用

Protective effect of rhodiola rosea on rats with ischemic myocardial injury

目的探讨红景天对大鼠异丙肾上腺素性心肌缺血性损伤的保护作用。方法采用异丙肾上腺素(ISO)皮下注射制备SD大鼠心肌缺血性损伤模型,以红景天干预,曲美他嗪作为保护药物参照,50只SD大鼠随机分为5组:正常对照组(A)、ISO损伤组(B)、曲美他嗪组(C)、高剂量红景天组(D)及低剂量红景天组(E)。观察各组大鼠心肌组织病理改变,检测心肌iNOS mRNA水平的表达变化;分析iNOS蛋白质水平表达变化。结果与B组比较,红景天能够明显减轻ISO所致的心肌细胞病理损伤范围和程度,且保护作用与剂量呈正相关。心肌损伤时iNOS mRNA以及蛋白表达均明显增高,而红景天组表达则明显降低且高剂量组较低剂量组表达降低。曲美他嗪作为一种阳性对照药物可以明显减轻大鼠心肌缺血性损伤,其疗效与低剂量红景天相似。结论红景天在心肌缺血性损伤中的保护作用机制可能与其抑制iNOS表达增加有关。

Objective To investigate the protective effect of rhodiola rosea on rats with ische- mic myocardial injury, and its possible mechanisms. Methods Rat model of ischemie myocardial in- jury was adopted by the means of injecting isoproterenol subcutaneously. Fifty SD rats were randomly divided into five groups, control group （group A）, ISO damaging group （group B）, trimetazidine group （ group C）, large dose of rhodiola protective group （ group D） and small dose of rhodiola protec- tive group （group E）. Changes of myocardial pathology and serum CK-MB of the groups were observed and recorded. The pathological and ultrastructure changes of myocardium were observed. The expres- sions of iNOS mRNA were also examined. Meanwhile iNOS protein expressions in the myocardium of the groups were investigated. Results Compared with ISO damaging group, rhodiola has significant protective effect on the extent and degree of cardiomyocytes injured by ISO on pathology. Moreover, the effect is positively correlated with the dose of rhodiola. Besides, the expressions of iNOS mRNA and protein increased remarkably once myocardial ischemic injury occurred. In contrast, Rhodiola group downregulated the expression of iNOS. The expression of the high-dose group was lower than that of the low - dose group. In the study, we used trimetazidine as a positive control drug which could also reduce myocardial injury. The effect was similar to the small dose of rhldiola group. Conclusion Pro- tective mechanism of rhodiola rosea in ischemic injury may be related to its role in downregulating the expression of iNOS.