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抑制核因子κB对缺血再灌注大鼠心肌组织的保护作用 被引量:3

Protect effects of inhibiting NF-κB on the myocardial tissue in the rats of ischemia-reperfusion injury
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摘要 目的探讨丹参注射液对心肌组织的保护作用及其抑制NF-κB活化的可能机制。方法通过观察NF-κB抑制剂PDTC和丹参注射液处理的缺血再灌注(I/R)大鼠心肌,测定心肌组织MDA、MPO、SOD、NF-κB及ICAM-1、TGFβ1蛋白表达。结果心肌匀浆MDA含量、MPO活力明显高于对照组(P<0.01),SOD活性显著低于对照组(P<0.01);PDTC和丹参注射液组,MDA含量、MPO活性较I/R组明显减少(P<0.01),SOD较I/R组明显恢复(P<0.01)。I/R组心肌细胞中NF-κBp65与ICAM-1蛋白表达信号显著增强,TGFβ1表达信号减低;在PDTC和丹参注射液组,NF-κBp65与ICAM-1表达水平较IR组明显降低,而TGFβ1呈相反变化。结论丹参注射液能增加I/R大鼠心肌SOD活性,减少脂质过氧化物MDA产生。减弱心肌MPO活力,减轻中性粒细胞对心肌细胞的浸润损害,抑制NF-κB的活化,保护I/R大鼠心肌组织。 Objective To investigate the myocardial protection function of Danshen drug injection (DI) and its possible mechanism for inhibiting NF-κB activation. Methods The cardiac muscle in the rats of ischemia-reperfusion(I/R) injury were treated by NF-κB inhibitor PDTC and Danshen injection to determine the MDA, MPO, SOD, NF-κB and protein expression of ICAM-1 and TGFβ1 Results The myocardial homogenate MDA content and MPO activity in experimental group were obviously higher than those in control group (P 〈 0. 01 ). The activity of SOD was significantly lower than that of control group ( P 〈 0. 01 ). In the PDTC group and MDA group, MDA content and MPO activity were obviously lower than that in I/R group( P 〈 0. 01 ), SOD recovered obviously than that in the latter group (P 〈 0. 01 ). In the myocardial cells of I/R group, NF-κB p65 and ICAM-1 protein expression signals enhanced obviously, TGFβ1 expression signals reduced. In PDTC and DI group,NF-κB p65 and ICAM-1 protein expression level was obviously lower than that of IR group,while TGFβ1 turned on the opposite change. Conclusions Danshen injection can increase SOD activity of I/R rat cardiac muscle,decrease lipid peroxidation substance MDA production,attenuate myocardial MPO activity,lessen infiltrating injury of neutrophilic granulocytes to the cardiac muscles, inhibit NF- κB activation,protect the rat myocardial tissue in I/R injury.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2007年第8期705-707,共3页 Chinese Journal of Gerontology
基金 辽宁省教育厅科技攻关课题(编号202013142)
关键词 缺血再灌注 核因子ΚB 吡咯基二硫氨基甲酸酯 黏附分子-1 转化生长因子Β1 Ischemia-reperfusion Nuclear factor kappa B(NF-κB) Pyrrolidine dithiocarbamate(PDTC) Intercellular adhesion molecule-1 ( ICAM-1 ) Transforming growth factor β1 ( TGFβ1 )
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