文献类型：期刊文献

中文题名：红芪黄酮在不同时间点对肺间质纤维化模型大鼠微血管新生指标的影响

英文题名：Effects of Hedysari Radix Flavonoids in Different Time Points on Angiogenesis Index in Pulmonary Interstitial Fibrosis Rat Model

作者：李娟[1];苏韫[1];张毅[1];刘永琦[1];舍雅莉[1];程小丽[1];李金田[1]

第一作者：李娟

机构：[1]甘肃中医学院敦煌医学与转化教育部重点实验室中药药理与毒理学省级重点实验室,兰州730000

第一机构：甘肃中医药大学科研实验中心（甘肃省中医药标准化技术委员会秘书处）

年份：2014

卷号：20

期号：3

起止页码：129

中文期刊名：中国实验方剂学杂志

外文期刊名：Chinese Journal of Experimental Traditional Medical Formulae

收录：CSTPCD;;北大核心:【北大核心2011】；

基金：国家自然科学基金地区科学基金(30960037/C020409);2004年教育部春晖计划项目(Z2004-1-620039);2010年度甘肃中医学院中青年基金(2010-2)

语种：中文

中文关键词：肺纤维化;红芪黄酮;微血管新生;血管内皮生长因子;血管内皮生长因子受体

外文关键词：pulmonary fibrosis; Hedysari Radix flavonoids; neovascularization; vascular endothelial growth factor; vascular endothelial growth factor receptor

摘要：目的:探讨红芪黄酮在不同时间点对肺间质纤维化模型大鼠微血管新生指标的影响。方法:SPF级Wistar大鼠144只,分为空白组、模型组、强的松组、红芪黄酮高、中、低剂量组,采用博莱霉素气管滴入方法建立肺纤维化模型,从造模后第2天起,各药物组分别给予相应剂量药物,按时间点连续灌胃治疗14,28 d,免疫组化法观察微血管内皮生长因子(VEGF)及其受体(VEGFR2)表达。结果:14,28 d模型组大鼠肺组织VEGF,VEGFR2表达较空白组明显增强(P<0.05,P<0.01),14 d红芪黄酮高剂量组大鼠肺组织VEGF,VEGFR2表达较14 d模型组减弱(P<0.05)。28 d红芪黄酮高剂量组VEGF,VEGFR2表达水平较28 d模型组减弱(P<0.05)。14,28 d红芪黄酮低剂量组VEGF、VEGFR2表达较28 d模型组相近。14,28 d红芪黄酮中剂量组VEGF,VEGFR2表达介于14,28 d高剂量组与低剂量组之间,但与14,28 d模型组相较无统计学意义。结论:红芪黄酮抗纤维化的作用机制可能是通过抑制微血管新生相关促进因子(VEGF及VEGFR2),进而抑制了病理性微血管的生成,而达到了延缓肺纤维化的作用。
Objective： To study the effect of Hedysari Radix flavonoids in different time points on angiogenesis index in the pulmonary interstitial fibrosis rat model. Method： Hundred and forty-four SPF Wistar rats were distributed to blank group, model group, prednisone group, Hedysari Radix flavonoids high, middle, low dose groups by bleomycin intratracheal instillation method to establish the model of pulmonary fibrosis. From the second day after modeling, the corresponding drugs were given to each group, ig for 14 days or 28 days. Immunohistochemistry method was used to observe the expression of vascular endothelial growth factor （VEGF） and its receptor （VEGFR2）. Result： Model groups 14, 28 days VEGF and VEGFR2 increased significantly when compared with the control group. Compared with 14 d model group, high dose flavonoids group in VEGF and VEGFR2 expression decreased （P 〈 0.05）. Compared with 28 d model group, high dose flavonoids group in VEGF and VEGFR2 expression decreased significantly （P 〈 0.05）. Fourteen, 28 d low dose groups had no significant difference with the 28 d model group, in VEGF and VEGFR2 expression. 14, 28 d middle dose groups in expression of VEGF and VEGFR2 were between 14, 28 d high dose group and low dose group, and had no statistical significance with 14 d, 28 d model group. Conclusion： The anti fibrosis mechanism of Hedysari Radix flavonoids was probably through inhibiting angiogenesis related factor VEGF and VEGFR2 to inhibit the formation of pathological angiogenesis resulting in the delayed pulmonary fibrosis.