三七总皂甙抗病毒性心肌炎慢性期小鼠心肌纤维化作用及其机制的研究  

Effects and Mechanisms of PNS on Myocardial Fibrosis in Chronic Viral Myocarditic Mice

作　　者：程志清[1] 徐百鸿[1] 窦丽萍[2] 刘旺[1] 王娟[1] 

机构地区：[1]浙江中医药大学基础医学院,杭州310053 [2]浙江中医药大学附属第二医院

出　　处：《浙江中医药大学学报》2008年第1期23-26,29,共5页Journal of Zhejiang Chinese Medical University

基　　金：浙江省医药卫生科学研究基金资助项目(No:2005A076)~~

摘　　要：[目的]探讨三七总皂甙(PNS)抗病毒性心肌炎慢性期小鼠心肌纤维化的作用及其可能的机制。[方法]通过反复感染柯萨奇病毒建立病毒性心肌炎慢性期小鼠模型,采用HE和VG染色观察心肌病变和纤维增生情况,采用病理检验方法对心肌胶原容积分数(CVF)和心肌血管周围胶原面积(PVCA)进行检测,并采用免疫组化法及RT-PCR法检测心肌中TGF-β1蛋白及其mR-NA表达水平。[结果]病毒性心肌炎慢性期模型组小鼠心脏出现明显心肌纤维化,与正常组比较,CVF和PVCA均显著增加(P<0.01),模型组心肌中TGF-β1蛋白及其mRNA表达水平均较正常组明显升高,与正常组比较,差异有显著性意义(P<0.01);三七总皂甙治疗组可以减轻心肌病变程度,CVF和PVCA示三七总皂甙各治疗组心脏中胶原比模型组均明显减少,并且三七总皂甙治疗组心肌中TGF-β1蛋白及其mRNA表达水平较模型组下降。[结论]三七总皂甙能下调病毒性心肌炎慢性期TGF-β1的表达,抑制心肌胶原的增生,提示其抗病毒性心肌炎慢性期心肌纤维化的作用可能部分通过抑制PDGF-BB过度表达有关。[Objective]To study the mechanisms and effects of panax notoginsenosides（PNS） on myocardial fibrosis in chronic viral myocarditic（VMC） mice. [Methods]The model mice with VMC at chronic status were established by repetitive infection of Coxsckievirus B3m（CVB3m）. Heart changes of myocardium and collagen hyperplasia were observed by HE and VG stain. Collagen volume fraction （CVF） and perivascular circuferential area （PVCA） were examined by pathological examination with computed processing. Myocardium TGF-β1 was detected by immunohistochemical method and mRNA expression of TGF-β1 was analyzed by Reverse transcription polymerase chain reaction （RT-PCR） method. [Results] Marked myocardial fibrosis was observed in chronic VMC model group. Compared with blank group, the index of CVF and PVCA was increased significantly（ P〈0. 01 ）. TGF-β1 immunohistochemical staining and TGF-β1 mRNA levels in VMC model group was significantly increased than the blank group（P〈0.01 ） ; Compared with chronic VMC model group, pathological changes of myocardium relieved in PNS treated group. The index of CVF and PVCA was decreased in PNS treated group. Further, TGF-β1 immunohistochemical staining and TGF-β1 mRNA levels in PNS- treated group were decreased than chronic VMC model group. [Conclusion]PNS inhibit TGF-β1 protein and mRNA over-expression in myocardium of chronic VMC mice, and reduce collagen synthesis, suggesting that its mechanism may be partly inhibiting TGF-β1 protein and mRNA over-expression in myocardium.

关 键 词：三七总皂甙 心肌纤维化 转化生长因子 病毒性心肌炎 

分 类 号：R285.5[医药卫生—中药学]