Effects of truncation and inversion prescription on the ultrastructure,Cyclin E and its transcription factor DP-1 in rats with ACLF

doi:10.3969/j.issn.1002-7386.2015.09.01

Abstract：Objective To observe the effects of truncation and inversion prescription on the ultrastructure,Cyclin E and its transcription factor DP-1 in liver cells of model rats with acute-on-chronic liver failure (ACLF), to explore 24-hour mortality and survival time of rat models and to analyze the therapeutic effects and action mechanism of the prescription on ACLF.Me thods Sixty -one Wistar rats were randomly divided into three groups: normal control group, model group and Chinese traditional medicine group (TCM group).The rat models with hepatic fibrosis or hepatic cirrhosis were established by immune induction of pig serum,then D-GalN/LPS one-time combination intraperitoneal injection was performed to establish the rat models with acute hepatic failure.After the animal models were established,the rats were treated by truncation and inversion prescription decoction through gavage for 3 days,then the rats in model group and TCM group were sacrificed respectively at 4h,8h,12h,and the ultrastructure changes of liver tissues were observed by electron microscopy, and the expression levels of Cyclin E and its transcription factors DP-1 were detected by ELISA.The images were analyzed by IPP6.0 software, and IOD value in positive substance was automatically calculated.Results The survival time in TCM group was significantly longer than that in model group ( P <0.05), furthermore,the ultrastructural injury of liver cells in TCM group was relieved at some extent; the IOD vlue and levels of Cyclin E ,DP-1 in TCM group at 8h were obviously lower than those at 4h,however,which in 12h were significantly increased,as compared with those at 8h ( P <0.01),but IOD value and levels of Cyclin E, DP-1 in model group were decreased continually.Conclusion Truncation and inversion prescription can prolong survival time of model rats, and can improve the ultrastructure of liver cells, which has regulative effects on compensatory proliferation of liver cells at some extent.