Heart Research Center of Chonnam National University Hospital, Gwangju 501-757, Republic of Korea.
Kidney Blood Press Res. 2013;37(4-5):229-39. doi: 10.1159/000350148. Epub 2013 Jul 8.
Background : Inhibition of histone deacetylase (HDAC) was reported to suppress cardiac hypertrophy and fibrosis in various hypertrophic animal models. However, the HDAC expression profile and HDAC enzyme activity have not yet been investigated in DOCA-salt hypertensive rats. Methods : Unilaterally nephrectomized rats were implanted with DOCA strips. DOCA-salt rats then received a control diet with vehicle or valproate. We measured the expression of cardiac hypertrophic markers, class I HDACs, class II HDACs, fibrosis, and HDAC enzyme activity. Results : Here we report that sodium valproate inhibits the cardiac hypertrophy accompanied by fibrosis in the heart of chronic hypertensive rats. We show that expression of GATA6 and HDAC6 is upregulated in DOCA-salt hypertension. In addition, HDAC6 and HDAC8 enzyme activity is attenuated by sodium valproate. Conclusion : These results suggest that a novel HDAC6- and HDAC8-selective inhibitor is needed to treat or prevent pathological cardiac hypertrophy. © 2013 S. Karger AG, Basel.
组蛋白去乙酰化酶(HDAC)的抑制被报道能抑制各种肥厚动物模型中的心肌肥厚和纤维化。然而,在 DOCA-盐性高血压大鼠中尚未研究 HDAC 的表达谱和 HDAC 酶活性。方法:单侧肾切除大鼠被植入 DOCA 带。然后,DOCA-盐大鼠接受含有载体或丙戊酸钠的对照饮食。我们测量了心脏肥厚标志物、I 类 HDAC、II 类 HDAC、纤维化和 HDAC 酶活性的表达。结果:我们在此报告丙戊酸钠抑制慢性高血压大鼠心脏中的心肌肥厚伴纤维化。我们表明 GATA6 和 HDAC6 的表达在 DOCA-盐性高血压中上调。此外,丙戊酸钠减弱了 HDAC6 和 HDAC8 的酶活性。结论:这些结果表明需要一种新型的 HDAC6 和 HDAC8 选择性抑制剂来治疗或预防病理性心肌肥厚。© 2013 S. Karger AG, Basel.