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1. 重庆医科大学第一附属医院眼科,重庆市眼科重点实验室,重庆市眼科研究所
2. 郑州大学人民医院,河南省人民医院,河南省立眼科研究所,河南眼科医院
纸质出版日期:2019,
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[1]麦雨欣,王罗梓怡,余鹏,刘彦尧,雷博.TO90可通过ACE2/Ang-(1-7)/MAS受体轴减轻Ang Ⅱ诱导人视网膜色素上皮细胞产生的炎症反应[J].第三军医大学学报,2019,41(20):1932-1938.
MAI Yuxin, WANG Luoziyi, YU Peng, et al. TO90 inhibits angiotensin Ⅱ-induced inflammatory response by up-regulating ACE2/Ang-(1-7)/MAS receptor axis in human retinal pigment epithelial cells[J]. Journal of Army Medical University, 2019,41(20):1932-1938.
[1]麦雨欣,王罗梓怡,余鹏,刘彦尧,雷博.TO90可通过ACE2/Ang-(1-7)/MAS受体轴减轻Ang Ⅱ诱导人视网膜色素上皮细胞产生的炎症反应[J].第三军医大学学报,2019,41(20):1932-1938. DOI: 10.16016/j.1000-5404.201905190.
MAI Yuxin, WANG Luoziyi, YU Peng, et al. TO90 inhibits angiotensin Ⅱ-induced inflammatory response by up-regulating ACE2/Ang-(1-7)/MAS receptor axis in human retinal pigment epithelial cells[J]. Journal of Army Medical University, 2019,41(20):1932-1938. DOI: 10.16016/j.1000-5404.201905190.
目的探讨TO90与ACE2/Ang-(1-7)/MAS受体轴在血管紧张素Ⅱ(angiotensinⅡ
AngⅡ)诱导的人视网膜色素上皮细胞(retinal pigment epithelium cells
ARPE-19)炎症反应中的关系。方法体外培养ARPE-19细胞
首先将其分为空白对照组及AngⅡ模型组(1μmol/L AngⅡ刺激细胞48 h)
Real-time PCR与ELISA检测慢性低度炎症因子IL-6、IL-8、MCP-1的表达
判断是否成功建立炎症模型。随后将ARPE-19细胞分为AngⅡ模型组与TO90+AngⅡ治疗组
重复之前步骤检测慢性低度炎症因子IL-6、IL-8、MCP-1表达;Real-time PCR及Western blot检测ACE2及MAS受体表达
探究TO90在AngⅡ炎症模型中的作用。最后将ARPE-19细胞分为AngⅡ模型组、TO90+AngⅡ治疗组、A779(MAS受体抑制剂)+TO90+AngⅡ抑制剂组以及A779+AngⅡ抑制剂对照组
Real-time PCR、ELISA及Western blot重复之前步骤检测慢性低度炎症因子IL-6、IL-8、MCP-1、ACE2及MAS受体的表达
进一步验证TO90在AngⅡ炎症模型中的作用。结果 AngⅡ刺激ARPE-19细胞后
IL-6、IL-8及MCP-1在mRNA及蛋白水平表达升高(P<0.05)
TO90预处理ARPE-19细胞能显著减少IL-6、IL-8及MCP-1在mRNA及蛋白水平的表达(P<0.05)
同时升高ACE2及MAS受体表达水平(P<0.05)。A779抑制后
与TO90+AngⅡ治疗组相比
IL-6、IL-8及MCP-1在mRNA及蛋白水平表达量均显著升高(P<0.05)
ACE2及MAS受体表达水平降低(P<0.05)。结论 TO90通过ACE2/Ang-(1-7)/MAS受体轴减轻AngⅡ诱导人视网膜色素上皮细胞产生的炎症反应
Objective To investigate whether TO90 inhibits angiotensin Ⅱ(Ang Ⅱ)-induced inflammatory response by regulating the expressions of ACE2/Ang-(1-7)/MAS receptor axis in human retinal pigment epithelial cells. Methods In vitro cultured ARPE-19 cells were treated with Ang Ⅱ for 48 h
and the changes in the expressions of interleukin-6(IL-6)
IL-8 and monocyte chemoattractant protein-1(MCP-1) were detected using real-time PCR and enzyme-linked immunosorbent assay(ELISA) to verify the establishment of the inflammatory cell model. The effect of TO90 on the inflammatory response of Ang Ⅱ-treated ARPE-19 cells was evaluated by detecting the expression of IL-6
IL-8
MCP-1
ACE2 and MAS receptor using real-time PCR and Western blotting. ARPE-19 cells treated with Ang Ⅱ
TO90+Ang Ⅱ
A779(a MAS receptor inhibitor)+TO90+Ang Ⅱ
or A779+Ang Ⅱ were examined for expressions of IL-6
IL-8
MCP-1
ACE2 and MAS receptors to further explore the effect of TO90 on Ang Ⅱ-induced inflammation response. Results Ang Ⅱ treatment resulted in significantly increased expressions of IL-6
IL-8 and MCP-1 at both the mRNA and protein levels in ARPE-19 cells(P<0.05)
and these effects were obviously attenuated by pretreatment of the cells with TO90(P<0.05)
which also caused significantly increased expressions of ACE2 and MAS receptor in the cells(P<0.05). In ARPE-19 cells treated with TO90+Ang Ⅱ
inhibition of MAS receptor with A779 significantly enhanced the expression of IL-6
IL-8
MCP-1
while inhibited the expression of ACE2 and MAS receptor at both the mRNA and protein levels(P<0.05). Conclusion TO90 inhibits Ang Ⅱ-induced inflammatory response by up-regulating the expressions of ACE2/Ang-(1-7)/MAS receptor axis in ARPE-19 cells.
TO90AngⅡ炎症反应ACE2MAS受体
TO90angiotensin Ⅱinflammatory reactionangiotensin-converting enzyme 2MAS receptor
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