淫羊藿苷预处理对心肌缺血再灌注损伤炎症反应的影响

Effects of icariin preconditioning on inflammatory responses in myocardial ischemia-reperfusion injury

目的：观察淫羊藿苷对心肌缺血再灌注损伤的影响并探讨是否存在剂量依赖关系.方法：结扎大鼠冠状动脉左前降支30 min,再灌注2 h,建立心肌缺血再灌注模型.将48只体重在250～300 g的健康成年雄性SD大鼠随机分为假手术组,模型组,淫羊藿苷低、中、高剂量组及阿司匹林组.HE染色观察心肌组织形态学改变,免疫组化法检测 NF-κB p65 蛋白在心肌细胞核中的表达,蛋白质免疫印迹法检测心肌组织中肿瘤坏死因子α（tumor necrosis factor α,TNF-α）表达,酶联免疫吸附法测定血清白细胞介素1β（interleukin 1β,IL-1β）含量,比色法检测心肌组织中髓过氧化物酶（myeloperoxidase,MPO）活性.结果：与假手术组比较,其余5组TNF-α表达及IL-1β浓度升高（P＜0.01）,NF-κB表达增强（P＜0.01）,MPO活性增加（P＜0.01）;与模型组比较,淫羊藿苷低、中、高剂量组及阿司匹林组TNF-α表达及IL-1β浓度下降（P＜0.05）,NF-κB表达减弱（P＜0.05）,MPO活性降低（P＜0.05）;淫羊藿苷高剂量组与阿司匹林组比较无显著差异（P＞0.05）.结论：淫羊藿苷预处理能减轻大鼠心肌缺血再灌注损伤炎症反应,并且呈现出剂量依赖性.

AIM： To observe the effects of icariin on myocardial ischemia-reperfusion injury. METHODS： The left anterior descending coronary artery was hgated for 30 min and then loosened for 2 h to establish the rat model of myocardial ischemia-reperfusion injury. Forty-eight healthy adult male SD rats weighing 250 ~ 300 g were randomly divided into sham group, model group, low-, middle-and high-dose icariin groups, and aspirin group. The morphological changes of the myocardium were observed by HE staining. The protein expression of NF-KB p65 in the myocardial nucleus was determined by the method of immunohistochemistry. The content of tumor necrosis factor α （TNF-α） in the myocardial tissues was detected by Western blotting. The level of interleukin 113 （IL-113） in the serum was measured by ELISA. The activity of myetoperoxidase （MPO） in the myocardial tissues was assayed by colorimetry. RESULTS ： Compared with sham group, TNF-α content, IL-1β concentration, NF-KB expression and MPO activity in all other groups increased. Compared with model group, TNF-α content, IL-1β concentration, NF-KB expression and MPO activity in low-, middle- and highdose icariin groups and aspirin group all decreased. No significant difference of the above parameters between high-dose icariin group and aspirin group was observed. CONCLUSION： Icariin preconditioning reduces inflammatory responses in the process of myocardial ischemia-reperfusion injury in a dose-dependent manner.