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双参通冠方对急性心肌缺血再灌注模型核因子-κB信号途径及细胞间隙连接通讯的影响 被引量:22

Effect of Shuangshen Tongguan Recipe on Nuclear Factor-kappa B Signal Pathway and Myocardial Junction-Mediated Intercellular Communication in Acute Myocardial Ischemia/Reperfusion Injured Model Rats
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摘要 目的观察双参通冠方 (SSTG)对急性心肌缺血再灌注损伤动物模型心肌梗死面积及重量 ,心肌核因子 κB(nuclearfactor- kappaB ,NF-κB)信号途径及心肌细胞间隙连接蛋白Cx4 3的影响。方法用冠状动脉结扎 /放松法复制大鼠心肌缺血再灌注损伤模型 ,N-BT染色法测量心肌梗死范围 ;免疫组织化学法检测心肌组织NF-κBp6 5表达 ;双抗体夹心ABC-ELISA法测定各组血清肿瘤坏死因子 (TNF α)和细胞间黏附分子- 1(ICAM-1)含量 ;免疫组织化学法测定心肌细胞通讯间隙连接蛋白Cx4 3表达。结果模型组大鼠心肌梗死面积及梗死区重量、NF-κBp6 5表达、血清中TNF-α及ICAM-1含量明显升高 (P <0.0 5 ) ;心肌连接蛋白Cx4 3大量降解。SSTG处理后心肌梗死面积及重量减轻 ;血清中TNF α、ICAM 1水平下调 (P <0 0 5 ) ;NF κBp6 5表达及Cx4 3降解抑制。 结论缺血再灌注时 ,心肌梗死严重 ,NF κB信号途径可被激活 ,Cx4 3降解严重。SSTG能抑制NF-κB的活化 ,抑制血清中TNF-α、ICAM-1的过量分泌和抑制Cx4 3的降解 。 investigate the effects of Shuangshen Tongguan Recipe (SSTG) on myocardial nuclear factor-kappa B (NF-κB) signal pathway, expression of myocardial junction intercellular communication (MJIC) connexin 43 (Cx43), and infarcted myocardial size and weight of the rats' heart after acute myocardial ischemia/reperfusion (I/R) damage. MethodsModel rat of I/R injury was established by coronary arterial ligating/releasing. The infarcted myocardial size and weight were determined by N-BT staining, expression of NF-κB p65 in myocardial tissue and Cx43 were determined by immunohistochemical method, contents of serum tumor necrosis factor-α(TNF-α) and intercellular adhesion molecule-1 (ICAM-1) were measured by ABC-ELISA. ResultsThe myocardial infarcted size and weight, expression of NF-κB p65, contents of serum TNF-α and ICAM-1 of I/R injured rats in the model group were significantly increased (P<0.05), while Cx43 degraded markedly after modeling. These changes were restored after treated with SSTG (P<0.05). ConclusionSerious myocardial infarction occurs after ischemia/reperfusion injury, combined with NF-KB signal pathway activation and severe Cx43 degradation. SSTG could inhibit the activation of NF-κB, the over-excretion of TNF-α and ICAM-1 in serum, and the degradation of Cx43 to decrease the myocardial infarcted size and weight.
出处 《中国中西医结合杂志》 CAS CSCD 北大核心 2005年第3期228-231,共4页 Chinese Journal of Integrated Traditional and Western Medicine
基金 国家"8 63"计划课题 (No .2 0 0 4AA2 2 381 2 )
关键词 双参通冠方 急性心肌缺血再灌注模型 核因子-κB信号途径 细胞间隙连接通讯 心肌梗死 Shuangshen Tongguan Recipe ischemia/reperfusion injury nuclear factor-κ B signal pathway tumor necrosis factor-α intercellular adhesion molecule-1 intercellular communication connexin 43
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  • 1Arenzana-Seiscledos E, Turpin P, Rodriguez M, et al. Nuclear localization of Ⅰ -кB promotes active transport of NF-кB from the nucleus to the cytoplasm. J Cell Sci 1997; 110(Pt 3) :369-378.
  • 2Li C, BrBwder W, Kao RI.. Early activation of transcription factor NF-кB during ischemia in perfused rat heart. Am J Physiol 1992 ; 276 : H543 - 552.
  • 3Baeuerle PA, Henkel T. Function and activiation of NF -кB in the immune system. Ann Rev Immunol 1994; 12: 141-179.
  • 4陈修 陈维洲 曾贵云.心血管药坪学[M].北京:人民卫生出版社,1998.117.
  • 5Peters NS. New insights into myocardial arrhyttnnogensis:distribution of gap-junctional coupling in normal, ischemie and hypertrophied hearts. Clin Sci (Lond) 1996 ; 9(3 ( 6 ) : 447-452.
  • 6Luke RA, Saffitz JE. Remodeling of ventricular conduction pathway in healed caine infarct border zones. J Clin Invest 1991 ;87(5) : 1594-1602.
  • 7Ikeda T, Yashima M, Uchida T, et al. Attachment of meandering reentrant wave fronts to anatomic obstacles in the atrium, role of the obstacle size. Circ Res 1997;81 (5) :753-764.

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