2005Unpublished venueRequires access

The role of HDAC 2 in pressure overload-induced cardiac hypertrophy of rat

Yin Lu

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Abstract

Objective To investigate the expression and the role of HDAC2 in the rat model of pressure overload -induced cardiac hypertrophy and the effect of valproic acid sodium on the expression of HDAC2 and the development of cardiac hypertrophy. Methods Male Wistar rats were divided randomly into sham-operated group,cardiac hypertrophy group and valproic acid sodium treatment group. All animals were sacrificed at 14 days and 28 days respectively. The heart/body weight ratio ,myocardium HE stain and the mRNA expression of β-MHC were observed. The expression of HDAC2 was examined by using RT-PCR and immunohistochemistry. Results The heart/body weight ratio and the level of β-MHC mRNA of treatment group decreased compared with cardiac hypertrophy groups; myocardium HE stain showed that the extent of myocardial injury in cardiac hypertrophy group was more serious than that in the treatment groups; The number of positive nucleus in per high power field of treamtment groups for 14 days and 28 days decreased by 34.18% and 36.24% respectively compared with those of cardiac hypertrophy groups, P 0.05. Conclusions The expression of HDAC2 may play an important role in cardiac hypertrophy. Valproic acid sodium may inhibit the expression of HDAC2 and the development of cardiac hypertrophy.[

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Objective To investigate the expression and the role of HDAC2 in the rat model of pressure overload -induced cardiac hypertrophy and the effect of valproic acid sodium on the expression of HDAC2 and the development of cardiac hypertrophy. Methods Male Wistar rats were divided randomly into sham-operated group,cardiac hypertrophy group and valproic acid sodium treatment group. All animals were sacrificed at 14 days and 28 days respectively. The heart/body weight ratio ,myocardium HE stain and the mRNA expression of β-MHC were observed. The expression of HDAC2 was examined by using RT-PCR and immunohistochemistry. Results The heart/body weight ratio and the level of β-MHC mRNA of treatment group decreased compared with cardiac hypertrophy groups; myocardium HE stain showed that the extent of myocardial injury in cardiac hypertrophy group was more serious than that in the treatment groups; The number of positive nucleus in per high power field of treamtment groups for 14 days and 28 days decreased by 34.18% and 36.24% respectively compared with those of cardiac hypertrophy groups, P 0.05. Conclusions The expression of HDAC2 may play an important role in cardiac hypertrophy. Valproic acid sodium may inhibit the expression of HDAC2 and the development of cardiac hypertrophy.[

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Available abstract

Objective To investigate the expression and the role of HDAC2 in the rat model of pressure overload -induced cardiac hypertrophy and the effect of valproic acid sodium on the expression of HDAC2 and the development of cardiac hypertrophy. Methods Male Wistar rats were divided randomly into sham-operated group,cardiac hypertrophy group and valproic acid sodium treatment group. All animals were sacrificed at 14 days and 28 days respectively. The heart/body weight ratio ,myocardium HE stain and the mRNA expression of β-MHC were observed. The expression of HDAC2 was examined by using RT-PCR and immunohistochemistry. Results The heart/body weight ratio and the level of β-MHC mRNA of treatment group decreased compared with cardiac hypertrophy groups; myocardium HE stain showed that the extent of myocardial injury in cardiac hypertrophy group was more serious than that in the treatment groups; The number of positive nucleus in per high power field of treamtment groups for 14 days and 28 days decreased by 34.18% and 36.24% respectively compared with those of cardiac hypertrophy groups, P 0.05. Conclusions The expression of HDAC2 may play an important role in cardiac hypertrophy. Valproic acid sodium may inhibit the expression of HDAC2 and the development of cardiac hypertrophy.[

Key concepts: Internal medicine, Muscle hypertrophy, Histone deacetylase 2, Endocrinology, Valproic Acid, Medicine, Cardiac muscle, Immunohistochemistry

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