黄芩苷抑制大鼠血管平滑肌细胞增殖和新生内膜肥厚  

Baicalin inhibits VSMC proliferation and neointimal hyperplasia in rats

作　　者：呼海娟[1] 韩梅[1] 孙荣华[1] 刘彬[1] 温进坤[1] 

机构地区：[1]河北医科大学基础医学研究所,河北石家庄050017

出　　处：《基础医学与临床》2010年第12期1252-1256,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(30770787);河北省自然科学基金(C2007000831)

摘　　要：目的探讨黄芩苷对大鼠血管平滑肌细胞(VSMC)增殖和内皮损伤诱导的新生内膜形成的影响及其机制。方法采用细胞培养、MTT分析、Western blot及免疫组织化学等方法研究黄芩苷的作用机制。结果黄芩苷可呈浓度依赖性地抑制血小板源生长因子(PDGF)诱导的VSMC增殖,降低增殖细胞核抗原(PCNA)的表达,阻断PDGF受体的激活和MEK/ERK信号通路的活化。整体实验显示,黄芩苷可预防球囊损伤诱导的血管新生内膜肥厚,明显降低内膜/中膜面积(I/M)比值(P<0.01);PCNA、细胞间黏附分子(ICAM-1)和血管黏附分子(VCAM-1)蛋白的表达也明显减少(P<0.01)。结论黄芩苷通过抑制VSMC增殖而阻止球囊损伤诱导的大鼠血管内膜增生。Objective To elucidate the effect of baicalin on proliferation of vascular smooth muscle cells（VSMCs） and neointimal hyperplasia after balloon injury and the potential mechanism.Methods Cell culture,MTT assay,Western blot and immunohistochemical staining were adopted to evaluate the inhibitory effects of baicalin on VSMC proliferation.Results Baicalin inhibited cell proliferation induced by PDGF in a dose-dependent（5,10,20,40 μmol/L） manner,reduced proliferating cell nuclear antigen（PCNA） expression and blocked PDGFR-MEK-ERK1/2 signaling pathway activated by PDGF in VSMCs.In vivo,baicalin significantly inhibited neointimal hyperplasia induced by balloon injury.The ratio of intima-to-media area（I/M） in baicalin group was significantly less than that in balloon injury group（P0.01）.The expressions of PCNA,ICAM-1 and VCAM-1 were significantly reduced in baicalin group as compared with the balloon injury group.ConclusionBaicalin inhibits neointimal hyperplasia via inhibiting VSMC proliferation and adhesion molecule expression induced by balloon injury.

关 键 词：黄芩苷 血管平滑肌细胞 增殖 内膜肥厚 

分 类 号：R285.5[医药卫生—中药学]