缺氧诱导因子-1对大鼠缺血再灌注损伤后急性炎症应答的影响

发布时间：2018-05-05 14:46

本文选题：心肌缺血再灌注损伤 + 缺氧诱导因子-　；参考：《中外医疗》2009年22期

【摘要】：目的观察缺氧诱导因子-1对大鼠心肌缺血再灌注损伤后急性炎症应答的影响。方法健康清洁级大鼠24只,随机分为3组:二甲基乙二酰基甘氨酸(TMOG)组、对照组、假手术组,每组8只。TMOG组,在缺血与再灌注损伤模型建立前24h进行腹腔内注射20ug/gTMOG;对照组,在缺血与再灌注损伤模型建立前24h进行腹腔内注射生理盐水0.5mL;除假手术组,其余2组通过结扎冠状动脉左前降支60min,然后松开180min建立心肌缺血再灌注损伤动物模型;假手术组不结扎冠状动脉左前降支。3组大鼠均在实验终点采右心房血,分离血清,测定血清中的细胞间粘附分子-1(ICAM-1)、白细胞介素-8(IL-8)的表达水平;处死动物取出心脏,测定大鼠心肌组织的缺氧诱导因子-1的mRNA表达。结果TMOG组缺氧诱导因子-1的mRNA表达比对照组明显增多(P0.05);TMOG组血清中的ICAM-1及IL-8的表达水平明显降低(P0.05)。结论缺氧诱导因子-1能通过抑制ICAM、IL-8的合成,减少中性粒细胞的浸润,从而改善心肌缺血再灌注损伤,对心肌缺血再灌注损伤具有重要保护作用,为防治心肌缺血再灌注损伤提供了新的治疗思路。
[Abstract]:Objective to observe the effect of hypoxia inducible factor-1 (HIF-1) on acute inflammatory response after myocardial ischemia reperfusion injury in rats. Methods Twenty-four healthy clean grade rats were randomly divided into three groups: dimethyl acetylglycine (TMOG) group, control group, sham-operated group, 8 rats in each group. 24 hours before the establishment of ischemia and reperfusion injury model, 20uggTMOG was injected intraperitoneally in the control group. 0.5 mL saline was injected intraperitoneally 24 hours before the establishment of ischemia and reperfusion injury model, the other two groups were ligated the left anterior descending coronary artery for 60 minutes, then released 180min to establish myocardial ischemia-reperfusion injury animal model. In the sham operation group, the right atrial blood was collected from the left anterior descending coronary artery at the end of the experiment, the serum was isolated, and the expression of intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) in the serum were determined. The expression of hypoxia inducible factor-1 (mRNA) in rat myocardium was determined. Results the mRNA expression of hypoxia inducible factor-1 in TMOG group was significantly higher than that in control group. The expression of ICAM-1 and IL-8 in serum of TMOG group was significantly lower than that of control group. Conclusion Hypoxia-inducible factor 1 can reduce the infiltration of neutrophils by inhibiting the synthesis of IL-8 in ICAM, thus improving myocardial ischemia-reperfusion injury, and has an important protective effect on myocardial ischemia-reperfusion injury. It provides a new therapeutic idea for prevention and treatment of myocardial ischemia reperfusion injury.
【作者单位】：福建中医学院附属人民医院检验科;福建医科大学;福建省立医院心血管病重点实验室研究所;福建中医学院附属人民医院ICU室;
【分类号】：R363

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