摘要
目的:观察丹参酮ⅡA(STS)对交感神经系统介导的心肌细胞炎症反应的作用研究。方法:原代培养大鼠心肌细胞,使用不同浓度STS干预血管紧张素Ⅱ(AngⅡ)刺激的心肌炎症反应,Real-time PCR及ELISA方法测定心肌细胞TLR4、TNF-α mRNA表达及细胞培养上清液TNF-α浓度,Western blot检测细胞浆蛋白IκB-α及细胞核蛋白NF-κB p65表达。结果:不同浓度STS干预后,心肌细胞TLR4、TNF-α mRNA表达及TNF-α浓度下降,心肌细胞浆蛋白IκB-α水平下降及核蛋白NF-κB p65水平升高,随着干预浓度的升高,这种作用逐渐增强。结论:STS对AngⅡ刺激心肌细胞引起的炎症反应有良好的保护作用,其机制与抑制细胞内NF-κB激活,减少炎性因子分泌有关。
Objective:To observe the effect of sodium tanshinone ⅡA sulfonate on the inflammatory reaction mediated by the sympathetic nervous system in cardiomyocytes. Method:The primary myocardial cells were cul- tured in vitro. Different concentration of tanshinone ⅡA were performed to intervene the inflammatory response induced by angiotensin Ⅱ. The expression of TLR4 and TNF-a mRNA were detected by real time PCR,and the level of TNF-a was measured by ELISA, and the expression of IgBa and NF-kB p65 were detected by Western blot. Result: The expression of TLR4 and TNF-a mRNA in cardiomyocytes,as well as the concentration of TNF-a in cell culture supernanant decreased. And the levels of myocardial plasma protein I kappa B alpha decreased and the levels of nuclear protein NF-kappa B p65 increased after application of the different concentration of tanshinone Ⅱ A,and this effect was in a concentration-dependent manner. Conclusion: Sodium tanshinone Ⅱ A sulfonate has a positive effect on the inflammatory response induced by Ang Ⅱstimulation in cardiomyocytes,and its mechanism might related to the inhibition of NF-kB activation and the depression of secretion of inflammatory cytokines in the ceils.
出处
《临床急诊杂志》
CAS
2017年第4期285-288,共4页
Journal of Clinical Emergency
基金
湖北省武汉市临床医学科研项目(No:WX14C34)
关键词
心肌细胞
丹参酮ⅡA
血管紧张素Ⅱ
肿瘤坏死因子
cardiomyocytes
sodium tanshinone Ⅱ A sulfonate
angiotensinⅡ
tumor necrosis factor