期刊文献+

替米沙坦对体外培养的人脐动脉平滑肌细胞表达ICAM-1和ET-1影响 被引量:1

Effect of telmisartan on ICAM-1 and ET-1 expressed by HUASMCs
原文传递
导出
摘要 目的:考察替米沙坦对体外培养的人脐带动脉血管平滑肌细胞(HUASMCs)表达细胞间黏附分子-1(ICAM-1)和内皮素-1(ET-1)影响,为临床应用替米沙坦治疗高血压等疾病提供参考。方法:采用组织块贴壁法培养HUASMCs。取传3代的细胞进行α-actin肌动蛋白免疫组化染色法鉴定。取传3代细胞,分别加入1,10,100μg·mL^(-1 )3种质量浓度替米沙坦细胞培养液,于加药后48 h进行试验。分别采用RT-PCR法和ELISA法,检测替米沙坦对HUASMCs表达ICAM-1和ET-1 mR-NA和蛋白的影响。结果:组织块贴壁法成功培养出HUASMCs,传第3代细胞呈现明显的HUASMCs特性。低、中、高3种作用浓度的替米沙坦均可抑制HUASMCs表达ICAM-1和ET-1 mRNA(P<0.05),也均可抑制HUASMCs表达ICAM-1和ET-1蛋白(P<0.05),且抑制作用均呈浓度依赖性(P<0.05)。结论:替米沙坦可使体外培养的HUASMCs表达ICAM-1和ET-1下调。 OBJECTIVE To investigate the effects of telmisartan on the expression of intercellular adhesion molecule-1(ICAM-1)and endothelin-1(ET-1)secreted by human umbilical arterial smooth muscle cells(HUASMCs)cultured in vitro against cardiovascular diseases.METHODS A tissue adherent method was used to culture HUASMCs.The third generation cells were detected byα-actin immunohistochemical staining and cultured with telmisartan at 1,10 and100μg·mL^-1,respectively to conduct the test 48 h later.RT-PCR method and ELISA method were used to determine the effects of telmisartan on mR-NA and protein of ICAM-1 and ET-1 expressed by HUASMCs.RESULTS Tissue adherent method was used successfully for cultivating HUASMCs of the third generation which showed typical characters of HUASMCs.The low,medium,high concentrations of telmisartan not only inhibited the expression of ICAM-1 and ET-1 mRNA in HUASMCs(P0.05),but also inhibited the ability of HUASMCs to secret the proteins of ICAM-1 and ET-1(P0.05)in a concentration dependent manner(P0.05).CONCLUSION Telmisartan can inhibit and down regulate both expression and secretion of ICAM-1 and ET-1 mRNA in HUASMCs cultured in vivo.
出处 《中国医院药学杂志》 CAS 北大核心 2017年第24期2432-2435,2447,共5页 Chinese Journal of Hospital Pharmacy
基金 黑龙江省博士后启动基金项目(编号:LRB05-230) 黑龙江省卫生计生委科研课题(编号:2014-324)
关键词 替米沙坦 人脐动脉平滑肌细胞 细胞间黏附分子-1 内皮素-1 telmisartan human umbilical arterial smooth muscle cells intercellular adhesion molecule-1 (ICAM-1) endothe-lin-1 (ET-1)
  • 相关文献

参考文献8

二级参考文献101

共引文献47

同被引文献11

引证文献1

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部