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Inhibitory Effect of Sodium Ferulate on the Cardiomyocyte Hypertrophy Induced by AngiotensionⅡ
Objective:To investigate the effects of sodium ferulate(SF) on myocardial hypertrophy of rat and explore the protective mechanism.Methods:The myocardial hypertrophy was induced by 0.1μmol·L-1 Ang II. The cytoactive was detected by MTT. The cultured cardiomyocytes from Sprague Dawley neonate rats were randomly divided into normal,model,L-arginine(L-arg 1000μmol·L-1) group and SF(50,100,200μmol·L-1) group.To observe whether SF had nonspecifi c injurious effect on the cells,SF 200μmol·L-1was added into the normal cardiomyocytes and to determine whether the effect of SF on cardiomyocyte hypertrophy was associated with NO release,another two groups were established. NG-nitro-L-arginine-methyl ester(L-NAME) 1500μmol·L-1 combined with SF 200μmol· L-1 or L-arg 1000μmol·L-1,respectively. Cardiomyocyte hypertrophy was confirmed by observing the histological changes and the measurements of cell diameter,protein content and ANF andβ-MHC mRNA expression of the cells.The levels of NO,NOS and eNOS activity,the contents of cGMP and cAMP. The expression of eNOS were detected by Real time PCR and Western blotting.Results:① SF (50,100,200μmol·L-1) had no obvious side effect on cultured neonatal rat cardiomyocytesin vitro. In the group added 0.1μmol·L-1AngⅡ alone,the cells displayed swollen,with undistinguishable border;the diameter and protein content of cardiomyocytes was increased remarkably,and the expression of ANF andβ-MHC mRNA were up-regulated by AngⅡ. SF and L-arg could ameliorate the cardiomyocyte hypertrophy which can be inhibit by L-NAME.② Compared with normal group, 0.1μmol· L-1Ang II could decrease the NO content,NOS and eNOS activity in supernatant of cultured cardiomyocytes,decrease the content of cGMP and increase the content of cAMP incardiomyocytes,up-regulation the expression of eNOS.SF-H and L-arg administrated could siginifi cantly ameliorate these changes.Conclusion:SF can inhibit cardiomyocyte hypertrophy induced AngⅡ in rats. The probable mechanism involved to promote NO-cGMP signaling pathway and up-regulate the expression of eNOS .
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阿魏酸钠对皮瓣缺血再灌注损伤保护作用机制的研究进展
皮瓣具有自身血供,又具有一定的厚度,因此在整形外科、骨科、创伤外科常使用皮瓣移植手术修复组织缺损畸形或用于器官再造,皮瓣在移植过程中,常出现缺血的过程,但当缺血的皮瓣恢复血流灌注后,有时反而出现部分或全部皮瓣坏死,严重影响手术疗效.研究表明,这主要是由于皮瓣缺血再灌注损伤(ischemia-reperfusion injury I-RI)所致.皮瓣缺血再灌注损伤的机制是由自由基、钙超载、白细胞等多因子介导的一系列复杂的病理生理过程,其具体机制尚未完全阐明[1].有研究证实,阿魏酸钠(sodium ferulate SF)具有清除自由基、抑制钙超载、抑制血小板聚集作用[2].本文就阿魏酸钠对皮瓣缺血再灌注损伤保护作用机制的研究进展综述如下.
