| [Objective]Viral myocarditis (VMC) is a common disease in children. Coxsackievirus B3 (CVB3) is an important pathogen that causes VMC, but the pathogenesis of VMC has been unknown until now. It is considered that virus could directly result in myocardial lesions at the early stage of VMC, and that a continuous virus infection and immunity destruction follow at the later stage of VMC. Few methods are effective on treating VMC up to now, while a lot of studies have proved that the treatment of traditional Chinese herbs is a new solution. Qiqin I is made from membranous milkvetch root, baikal skullcap root, etc. The efficacy of it is to clear away heat and toxic materials, to invigorate Qi and nourish Yin to activate blood circulation, and to dissipate blood stasis. The objective of this research was to investigate the therapeutic effect and mechanism of Qiqin I on CVB3-VMC in mice. [Methods]Firstly, the mice were divided into two groups at random: control group and drug toxicity group. Saline were perfused into micestomach in control group. The double therapeutic dosage of Qiqin I were perfused into mice stomach in drug toxicity group in order to observe acute toxicity.Secondly, BALB/c mice were infected (0.1ml) with 500TCID50CVB3, which were divided into three groups: viral control group, Qiqin I group, and the membranous milkvetch root group. The different drugs were given to Qiqin I group, and to membranous milkvetch root group. We detected LVP and LVdp/dtmax were detected at different time points, to observe myocardial lesions and to estimate myocardial histopathological scores. Ultrostructure of myocardial cell was observed when mice were killed at the 7th day after infection with 500TCID50CVB3, and mortality was recorded..Thirdly, we studied the role and mechanism of Qiqin I on prevention and cure CVB3 by cellular protected method.(1)CVB3 was inactivated directly. After Qiqin I of different concentrations and 100TCID50CVB3 were mixed for 3h, Hep-2 cell were infected by it for 1h, and CPE was observed;(2)Duplication of CVB3 was inhibited directly. After Hep-2 cell were attacked by 100TCID50CVB3 for 3h. Qiqin I of different concentration were added into it for lh, and CPE was observed;(3)Adsorption of CVB3 was inhibited. After Qiqin I of different concentrations was added for lh, Hep-2 cell was attacked by 100TCID50CVB3 for 3h, CPE was observed.We observed the expression levels of Qiqin I on TNF-a and the effect of Qiqin I on apoptosis. TdT -mediated dUTP nick and labeling (TUNEL) technique and immunohistochemistry staining were also used in the experiment.[Results]1 Survival rate of the experimental miceMortality rate reached the summit from the 7th day to the 10th day after the drugs were perfused into mice stomach. But, mice were alive after the 10th day. The survival rate of virus group, membranous milkvetch root group and Qiqin I group were 39.08%, 48.61% and 76.19 % respectively. The survival rate of Qiqin I group was increased significantly (P<0.05). After the 21st day, the survival rate of drug toxicity group reached 100%.2 Alteration of cardiac hemodynamics in MiceWe detected LVP and LVdp/dtwax at the 3rd, 5th and 7th day after BALB/c mice were infected with 500TCID50CVB3.(1)There was no significant difference in LVP between control group and virus group, but LVdp/dtmax of virus group decreased significantly (P<0.01). Both LVP and LVdp/dtmax of virus group decreased significantly at the 5th day and the 7th day (P<0.01)(2)Compared with virus group, LVdp/dtwax of membranous milkvetch root group increased significantly at the 5th day (P<0.05). And LVP and LVdp/dtmax of membranous milkvetch root group were higher than those of virus group at the 7th day (P<0.05)(3)Compared with virus group, LVP and LVdp/dtwax of Qiqin I group increased significantly in different time point (P<0.05). Even compared with membranous milkvetch root group, LVP of Qiqin I group increased significantly at the 5th day (P<0.05), and LVdp/dtmax of Qiqin I group increased significantly at the 5...
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