三七总皂苷对病毒性心肌炎慢性期小鼠心肌纤维化及细胞因子PDGF-B表达的影响

Effects and Mechanisms of PNS on Myocardial Fibrosis and Expression of PDGF-B in Chronic Viral Myoearditic Mice

目的:探讨三七总皂苷(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VC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PDGF-B蛋白及其mRNA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,心肌胶原容积分数CVF和心肌组织血管周围胶原面积PVCA均显著增加(P<0.01),模型组心肌中PDGF-B蛋白及其mRNA表达水平均较正常组明显升高,与正常组比较,差异有非常显著性意义(P<0.01);三七总皂苷治疗组可以减轻心肌病变程度,CVF和PVCA示三七总皂苷各治疗组心脏中胶原比模型组均明显减少,并且三七总皂苷治疗组心肌中PDGF-B蛋白及其mRNA表达水平较模型组下降。结论:三七总皂苷能下调病毒性心肌炎慢性期PDGF-B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-B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. Myocardlum PDGF - B was detected by immunohistochemical method and mRNA expression of PDGF - B 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 ） . PDGF- B immunohistochemical staining and PDGF - B 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 groups. The index of CVF and PVCA was decreased in PNS treated groups. Further, PDGF - B immunohistochemical staining and PDGF- B mRNA levels in PNS - treated groups was decreased than chronic VMC model group. Conclusion：PNS inhibit PDGF- B protein and mRNA over-expression in myocardium of chronic VMC mice,and reduce collagen synthesis. Suggesting that Its mechanism may be partly by inhibiting PDGF - B protein and mRNA over-expression in myocardium.