Shengmaisan Co Zhigancao Soup Subtraction Infected With Coxsackie B <sub> 3 </ Sub> Virus Cultured Rat Myocardial Cells

Viral Myocarditis (VMC) is a widespread cardiovascular disease that does harm to human health. It is comparatively satisfied at present that the traditional Chinese medicines treat the VMC. In this study, we investigated anti-viral effects and the protecting mechanisms of pulse-activating powder combined with the roast Glycyrrhiza decoction adjusted juice I and II for the cultured rat myocardial cells infected with Coxsackie virus B3 (CVB3). Myocardial cells, which were obtained from the ventricular myocardium of newborn Sparaque-Dawley rats to make the beating myocardial cells, were incubated for 48 hours and inoculated with 103TCD50 of B3 virus as experimental model of VMC. All drug directly were administrated to the culture medium of myocardial 3 cells in vitro. All models were randomly divided into six group: normal group, control group, positive interferon treated group, pulse-activating powder combined with roast Glycyrrhiza decoction adjusted juice (excluding Polygonum cuspidatum water exact) treated group(PGP I), Polygonum cuspidatum water exact treated group(PCE) and pulse-activating powder combined with roast Glycyrrhiza decoction adjusted juice (including Polygonum cuspidatum water exact) treated group(PGP II). Pathogenic changes and cells beating of normal myocardial cells and myocardial cells infected with CVB3 were observed by inverted microscope at 24,32, 48, 60 and 72 hours after viral inoculation, the ultrastructure of myocardial cells at 72 hours after virus inoculation was observed by electronic microscope, the activity of Lactate Dehydrogenase (LDH), Creatine Phosphate Kinase (CPK) were determined by biochemical semi-automatic analyzing instruments and the activity of LDH and Succinate Dehydrogenase (SDH) and glucogen granule were determined by cytochemical methods. The results showed that the PGP I, II and PCE significantly alleviated the pathogenic changes of myocardial cells infected with CVB3, improved the cell beating and percent of cell beating (compared with viral control 4 group, P < 0.05), alleviated the ultrastructive changes of myocardial cells; inhibited obviously from releasing enzyme of myocardial cells infected with CVB3 (compared with viral control group, P < 0.01); increased glucogen granule in myocardial cells, enhanced the activity of SDH and reduced the activity of LDH (compared with viral control group, P < 0.01). Effects of the PGP II were better than that of the PGP I and PCE(compared with control group P < 0.01). In this experiment, it is found that the PGP I ,II and. PCE have anti-viral effects for myocardial cells infected with CVB3 and significantly, protective effects for the changed myocardial cells infected with CVB3, and the stabilizing cell membrane and increasing the energy to cells probably is one of protective mechanism. Effects of the PGP II are better than that of PGP I and PCE, and therefore we suggest to treat the VMC with PGP II adding the PCE in clinic.