Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, PR China.
Biochem Biophys Res Commun. 2011 Sep 23;413(2):342-7. doi: 10.1016/j.bbrc.2011.08.101. Epub 2011 Aug 27.
Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS.
硫化氢 (H₂S) 在心血管生理学和疾病中起着至关重要的作用。然而，关于 H₂S 在心肌细胞肥大 (CH) 中的可能作用尚无信息。我们的结果表明，H₂S 供体 NaHS 预处理可显著减少[(3)H]-亮氨酸掺入、细胞表面积、脑利钠肽 (BNP)mRNA 表达、细胞内活性氧 (ROS)、miR-21 的表达，增加心肌肥厚细胞中心房利钠肽 (ANP)和 miR-133a 的表达。抗 miR-133a 抑制剂转染部分降低了 NaHS 的抗肥大作用。总之，H₂S 是 CH 的直接抑制剂；它通过增加 miR-133a 并抑制细胞内 ROS 的增加而起作用。
