文献类型：期刊文献

中文题名：参附注射液对心肌缺血再灌注老年大鼠NF-κB及IκB-α表达的影响

英文题名：Effects of ShenFu Injection on Expressions of NF-κB and IκB-α in Aged Rats with Myocardial Ischemia and Reperfusion

作者：薛建军[1];呼荟茹[2];齐兵献[2];张凌云[1];贾国龙[1]

第一作者：薛建军

机构：[1]甘肃省中医院,甘肃兰州730050;[2]甘肃中医学院

第一机构：甘肃省中医院,甘肃兰州730050

年份：2013

卷号：26

期号：2

起止页码：18

中文期刊名：西部中医药

外文期刊名：Western Journal of Traditional Chinese Medicine

收录：CSTPCD

基金：甘肃省自然科学研究基金(编号1010RJZA209)

语种：中文

中文关键词：心肌缺血再灌注;参附注射液;NF-κB;IκB-α

外文关键词：myocardial ischemia and reperfusion; ShenFu injection; NF-κB ;IK B-α

摘要：目的:探讨参附注射液对心肌缺血再灌注(I/R)老年大鼠心肌组织NF-κB及IκB-α的影响。方法:健康Wi st ar老年大鼠30只,18月龄,随机分为假手术组、模型组、参附组,每组10只。采用结扎左冠状动脉前降支法制备I/R模型。运用免疫组化方法观察I/R后心肌组织细胞中NF-κB及IκB-α蛋白表达;通过电镜观察心肌组织细胞结构变化情况。结果:与假手术组比较,模型组NF-κB表达明显增加(P<0.05),IκB-α表达明显下降(P<0.05);与模型组相比,参附组NF-κB表达明显下降(P<0.05),IκB-α表达明显增加(P<0.05)。电镜观察结果显示参附组心肌组织细胞结构受损明显减轻。结论:参附注射液可增加心肌组织中IκB-α的水平,减弱其降解作用,通过抑制NF-κB活性,从而阻断NF-κB调控的炎症反应及细胞凋亡,对I/R后心肌组织损伤起防治作用。
Objective： To explore the effects of ShenFu injection on NF-κB and IK B-α in aged rats with myocardial ischemia and reperfusion （I/R）. Method： Thirty aged rats were randomly divided into sham operation group （S group）, model group （I/R group） and ShenFu group （SF group）, ten rats each group. I/R models were established through ligation method of the left anterior descending coronary artery. The expressions of NF-κB and IK B-α in the cells of myocardial tissue were observed after I/R with immunohistochemical method; changes of cellular structure of myocardial tissue were explored with electron microscope. Result： Compared with S group, expressions ofNF-κB in I/R group increased obviously （P〈0.05）, expressions oflK B-α decreased notably （P〈 0.05）; compared with I/R group, the expressions ofNF-κB in SF group lowered obviously（P〈0.05）, expressions of IκB-α increased notably（P〈0.05）. The results of electron microscope revealed that the damage of cellular structure in the myocardial tissue of SF group was alleviated. Conclusion： ShenFu Injection could increase the level of IκB-α in the myocardial tissue, weaken its degradation, interrupt inflammatory reaction and cellular apoptosis regulated by NF-κB through inhibiting the activity ofNF-κB and prevent the damage of myocardial tissue after I/R.