文章摘要
俎常浩 吴淼 马静 刘韶 张赛丹.EMT 促进自发性高血压大鼠主动脉纤维化[J].,2015,15(19):3601-3604
EMT 促进自发性高血压大鼠主动脉纤维化
Endothelial-to-mesenchymal Transition Promotes AorticFibrosis in Spontaneously Hypertensive Rat
  
DOI:
中文关键词: 内皮间充质转化  自发性高血压大鼠  主动脉纤维化  氯沙坦  哌唑嗪
英文关键词: EMT  SHR  Aortic fibrosis  Losartan  Prazosin
基金项目:湖南省自然科学基金项目(12JJ5070)
作者单位
俎常浩 吴淼 马静 刘韶 张赛丹 中南大学湘雅医院心血管内科中南大学湘雅医院附属海口医院心血管内科中南大学湘雅医院药学部 
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中文摘要:
      目的:探讨内皮间充质转化(endothelial-to-mesenchymal transition, EMT)是否促进自发性高血压大鼠主动脉纤维化及降压治 疗对其干预作用。方法:将24只雄性自发性高血压大鼠(spontaneously hypertensive rats, SHR)随机分为SHR 组(S组,蒸馏水灌 胃)、哌唑嗪组(P 组,哌唑嗪5 mg/(Kg× d)灌胃)和氯沙坦组(L 组,氯沙坦10 mg/( Kg× d )灌胃),8 只雄性WKY 大鼠(W组,蒸馏 水灌胃)作为对照组,各组分别干预8 周后,通过Masson 染色检测各组大鼠主动脉纤维化程度,免疫荧光染色及Western Blot 检 测各组大鼠主动脉I型胶原、CD31 及FSP1 蛋白表达变化。结果:Western blot及Masson 染色显示从L组、P组到S 组大鼠主动脉 I型胶原含量依次增多,且主动脉壁厚度均显著大于W组(P<0.05),但P 组与L组大鼠主动脉管壁厚度无统计学差异(P=0.818);免 疫荧光染色表明,各组高血压大鼠主动脉均存在FSP1 及CD31共表达(FSP+CD31+)细胞,且从L 组、P 组到S组FSP+CD31+细胞 依次增多;Western Blot 检测表明,从W组、L 组、P 组到S组,CD31蛋白表达量逐渐降少,FSP1 蛋白表达量依次增加,差异有统 计学意义(P<0.05)。结论:EMT 可能参与了自发性高血压大鼠的主动脉纤维化,氯沙坦和哌唑嗪可能通过抑制EMT减轻主动脉 纤维化。
英文摘要:
      Objective:To investigate whether Endothelial-to-mesenchymal transition contributed to artery fibrosis in Spontaneously hypertensive rats(SHRs) and whether antihypertensive treatment could attenuate the effect.Methods:Wistar Kyoto (WKY) rats and spontaneously hypertensive rats were used in the experiment. 24 male SHRs were divided into three groups randomly, and received phosphate buffer, prazosin and losartan respectively, 8 male WKYs served as controls. 8 weeks later, all rats were sacrificed and their aortas were collected for further research. Masson trichrome stain was used to detect the deposition of collagen fiber, immunofluorescence was performed to evaluate cells that co-expressed CD31 and fibroblast specific protein-1(FSP-1), and Western Blot was applied to measure the expression of protein CD31, FSP-1 and collagen-Ⅰ .Results:Increased interstitial fibrosis was proved in SHRs’aortas both by Masson trichrome stain and Western Blot, while the phenomenon was diminished by the intervention of prazosin and losartan(P<0.05). The FSP+CD31+cells were found in all SHRs aortic immunofluorescence, FSP-1 and were markedly upregulated in SHRs, while CD31 was reduced significantly, and samely the phenomena were inhibited by prazosin and losartan.Conclusion:The fibrosis of SHRs’aortas may be induced, at least partially, by EMT. Meanwhile, EMT could be inhibited by the intervention of prazosin and losartan, and losartan was more effective than prazosin.
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