【Abstract】 Objective To investigate the effect of HDAC2 on the apoptosis of cardiac myocytes in rat heart failure model. Methods 40 healthy adult male (Sprague Dawley, SD) rats were randomly divided into HF group (20 rats), sham operation group (10 rats) and blank control group (10 rats, blank group). H & E staining was used for the analysis of cardiac gross morphology. QPCR was used to detect the expression level of HDAC2, HDAC3, HDAC4, mir199a 3P and their downstream gene p53. Western blot was used to detect the expression level of HDAC2 and p53 protein. The chromatin immunoprecipitation combined with PCR (chip PCR) was used to detect the binding level of HDAC2 and mir199a 3P promoter. Results Compared with sham group and blank group, myocardial cells in HF group were significantly hypertrophied. The levels of HDAC2 mRNA and p53 mRNA in HF group were significantly higher than those in sham group and blank group (P＜0.05). The level of mir199a 3P mRNA in HF group was significantly lower than that in sham group and blank group (P＜0.05). There was no significant difference in the expression levels of p53 mRNA, HDAC2 mRNA and mir199a 3P mRNA between sham group and blank group (P＞0.05). There was no significant difference in the expression level of HDAC3 and hdac4mrna between the groups (P＞0.05). The expression levels of HDAC2 protein and p53 protein in HF group were significantly higher than those in sham group and blank group (P＜0.05). There was no significant difference between sham group and blank group (P＞0.05). The binding level of HDAC2 and mir199a 3P promoter in HF group was significantly higher than that in sham group and blank group (P＜0.05), but there was no significant difference in the levels of HDAC3 and HDAC4 mRNA in each group (P＞0.05). Conclusion In the rat model of heartfailure, a histone deacetylase,medicates the tow expression of miR199a, which leads to the up regulation of p53, an apoptosis maker.