The purpose of this study is to investigate the differences of H3K27 trimethylation pattern between parthenogenetic and in vivo mouse (Mus musculus) embryos. The effect of trichostatin (TSA) on the level of H3K27me3 in parthenogenetic embryos, and the impact of TSA on parthenogenetic embryonic development were also studied. Firstly, we used the indirect immunofluorescence with specific antibody against H3K27me3 and showed that there was a mild intensity staining in the metaphase oocyte. We activated the metaphase oocytes by strontium chloride and then collected the embryos at different developmental stages. The in vivo embryos were collected by flushing the uterus at different times after injecting pregnant mare serum gonadotrophin and human chorionic gonadotropin. Different patterns of H3K27me3 staining were detected in normal fertilized embryos and parthenogenetic embryos. The relative fluorescence intensities of the different stage embryos were determined by laser scanning confocal microscopy. Moreover, the pronuclear embryos which were activated by strontium chloride were treated with TSA for 20 hours. The un-treated parthenogenetic embryos were cultured in a medium containing dimethyl sulfoxide (0.05%) as a control. The results showed that there was a trend of increasing fluorescence intensity in parthenogenetic embryos, reaching the highest in blastocysts, while it was opposite in the in vivo embryos from 2-cell to the blastocyst stage. However, the mean fluorescence intensity of the parthenogenetic embryos was generally lower than that of normal embryos. After the treatment with TSA, though there was no significant difference in early embryo development (P>0.05) between the treated and the non-treated groups, the level of H3K27me3 in parthenogenetic embryos increased. There was significant difference (0.015±0.002 vs.0.004±0.000 5,P<0.05) in blastocyst formation. These results indicated that the pattern of the H3K27me3 in parthenogenetic embryos differ significantly from that of the in vivo embryos, which may be one of the reasons causing the low development ability of the parthenogenetic embryos. The TSA treatment of parthenogenetic activation embryos causes a certain effect on the H3K27me3 pattern, improving the in vitro embryo development.