摘要
目的:探讨腹腔预注射全氟化碳(PFC)对大鼠缺血心肌的可能保护作用及机制。方法:将50只Wistar雄鼠随机平均分为5组,假手术组、缺血组、PFC低剂量组、中剂量组、高剂量组,采用结扎冠状动脉前降支造成大鼠心肌缺血损伤模型。用ELISA方法检测缺血20min、40min及60min时大鼠外周血中白细胞介素-6(IL-6)水平变化。行HE染色观察缺血心肌的病理变化,并用免疫组化方法检测心肌组织中核因子-κB(NF-κB)的激活情况。结果:各组外周血IL-6水平随着缺血时间延长呈逐渐升高趋势,缺血组与假手术组相比IL-6水平明显升高(P<0.05)。在40min和60min时,PFC量组与缺血组相比IL-6水平显著减少(P<0.05),但在20min时中剂量组与缺血组相比无明显统计学意义。剂量组与缺血组相比IL-6水平差别无统计学意义。高剂量PFC可减轻缺血心肌的组织形态学改变,有效抑制NF-κB的激活。结论:PFC可以降低外周血IL-6水平,减轻炎症反应,对缺血心肌起到一定的保护作用,其机制可能与PFC抑制NF-κB的信号传导通路有关。
Objective： To investigate the possible protective effect and mechanism of perfluorocarbon by intraperitoneal pre-injection in rats with myocardial ischemia. Methods： 50 male Wistar rats were randomly divided into 5 groups （10 rats/each group） ： the sham group, ischemia group, low dose group, middle dose group and high dose group. Ischemia was established by ligating left anterior descending coronary artery. The level of IL-6 in peripheral blood of each group was detected respectively by enzyme linked immunosorbent assay （ELISA） in different isehemic times （20min, 40min, and 60min）, and myocardium was assayed by Hematoxylin and Eosin （HE） staining to observe the pathological changes. Immunohistochemistry was carried out to investigate the activation of nuclear factor-kd. Results： The level of IL-6 increased gradually with ischemic time. Compared with sham group, the level of IL-6 was significantly increased （P〈0.05） in ischemia group; at 40min and 60min ischemic time points, the levels of IL-6 in middle dose group and high dose group were significantly lower than those in ischemia group （P〈0.05）, but at 20min ischemic time point, middle dose group had no statistical difference contrasted with ischemia group （P〉0.05）, low dose group had no statistical difference compared with ischemia group （P〉0.05） ; in contrast with ischemia group, middle and high dose PFC reduced the histopathological changes of myocardium and inhibited the activation of NF-xB effectively （P〈0.05）. Conclusion： PFC decreases the level of IL-6, inhibits inflammation reaction and protects ischemic myocardium to a certain degree, the protective mechanism may have connection with the function of PFC which can inhibit NF-kB signal transduction pathway.
出处
《国际心血管病杂志》
2011年第4期242-244,248,共4页
International Journal of Cardiovascular Disease
