Valproic acid inhibits cardiomyocyte hypertrophy and HDAC2 expressions induced by angiotensin II

AIM: To observe the expression of histone deacetylase 2 (HDAC2) in hypertrophic cardiomycytes induced by angiotensin II (AngII) and to study the inhibitory role of valproic acid (VPA). METHODS: Cultured cardiomyocytes were treated with AngII to induce hypertrophy, along with VPA of different concentrations. They were divided randomly into control group, hypertrophic group, and low (5×10-6 mol/L), medium (10-5 mol/L) and high concentration (2×10-5 mol/L) group. Morphological changes of cardiomyocytes were observed under the contrast phase microscope. mRNA levels of HDAC2 were examined by reverse transcriptase polymerase chain reaction (RT-PCR). Protein expressions of HDAC2 were examined by immunohistochemistry. RESULTS: Stimulated by AngII, cardiomyocytes were enlarged under the contrast phase microscope. After stimulation by AngII, the mRNA level of HDAC2 and the protein expression of HDAC2 increased in the hypertrophic cardiocytes. Along with VPA, these data decreased accordingly as the VPA concentrations increased. CONCLUSION: Expression of HDAC2 increased in hypertrophic cardiomyocytes stimulated by AngII. HDAC2 may play a role in cardiocyte hypertrophy. VPA may inhibit cardiomyocyte hypertrophy and HDAC2 expressions.