神经药理学报 ›› 2017, Vol. 7 ›› Issue (3): 62-62.
• 2017年全国老年痴呆与认知障碍相关疾病学术会议论文摘要—认知障碍及其他疾病相关研究 • 上一篇 下一篇
LUO Min1,2, Chen Pan-pan1,2, Yang Lu1, Shi Jing-shan1, Deng Jiang1*
摘要: 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 0.1 μmol•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 1000 μmol•L-1)group and SF(50, 100, 200 μmol•L-1) group.To observe whether SF had nonspecific injurious effect on the cells, SF 200 μmol•L-1was added into the normal cardiomyocytes and to determine whether the effect of SF on cardiomyocyte hypertrophy is associated with NO release, another two groups were established. NG-nitro-L-arginine-methyl ester (L-NAME) 1500 μmol•L-1 combined with SF 200 μmol•L-1 or L-arg1000 μmol•L-1, respectively. Cardiomyocyte hypertrophy was confirmed by observing the histological changes and the measurements of cell diameter, protein content and ANF and β-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, 200 μmol•L-1) had no obvious side effect on cultured neonatal rat cardiomyocytes in vitro. In the group added 0.1 μmol•L-1 Ang II alone, the cells displayed swollen, with undistinguishable border; the diameter and protein content of cardiomyocytes was increased remarkably, and the expression of ANF and β-MHC mRNA were up-regulated by Ang II. SF and L-arg could ameliorate the cardiomyocyte hypertrophy which can be inhibit by L-NAME. (2) Compared with normal group, 0.1 μmol • L-1 Ang 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 siginificantly ameliorate these changes.Conclusion: SF can inhibit cardiomyocyte hypertrophy induced Ang II in rats. The probable mechanism involved to promote NO-cGMP signaling pathway and up-regulation the expression of eNOS .