激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响

刘赟; 李敬诚; 尹延伟; 黎炳护; 郭露; 廖少琼; 曹小洁; 张明杰; 周毅; 陈磊; 龙春燕; 张莉莉

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激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响

论著 | 更新时间：2026-01-09

- 激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响
- Effect of TRPV1 activation on proliferation of vascular smooth muscle cells in spontaneously hypertensive rats
- 陆军军医大学学报 2015年37卷第8期页码：762-766
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  中图分类号： R322.12;R329.28;R544.102
- 纸质出版：2015
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刘赟,李敬诚,尹延伟,黎炳护,郭露,廖少琼,曹小洁,张明杰,周毅,陈磊,龙春燕,张莉莉.激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(08 ):762-766.　Liu Yun,Li Jingcheng,Yin Yanwei,Li Binghu,Guo Lu,Liao Shaoqiong,Cao Xiaojie,Zhang Mingjie,Zhou Yi,Chen Lei,Long Chunyan,Zhang Lili.Effect of TRPV1 activation on proliferation of vascular smooth muscle cells in spontaneously hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(08 ):762-766.

刘赟, 李敬诚, 尹延伟, et al. Effect of TRPV1 activation on proliferation of vascular smooth muscle cells in spontaneously hypertensive rats[J]. Journal of Army Medical University, 2015, 37(8): 762-766.
刘赟,李敬诚,尹延伟,黎炳护,郭露,廖少琼,曹小洁,张明杰,周毅,陈磊,龙春燕,张莉莉.激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(08 ):762-766.　Liu Yun,Li Jingcheng,Yin Yanwei,Li Binghu,Guo Lu,Liao Shaoqiong,Cao Xiaojie,Zhang Mingjie,Zhou Yi,Chen Lei,Long Chunyan,Zhang Lili.Effect of TRPV1 activation on proliferation of vascular smooth muscle cells in spontaneously hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(08 ):762-766. DOI：

刘赟, 李敬诚, 尹延伟, et al. Effect of TRPV1 activation on proliferation of vascular smooth muscle cells in spontaneously hypertensive rats[J]. Journal of Army Medical University, 2015, 37(8): 762-766. DOI：

摘要

目的探讨瞬时受体电位香草醛亚家族1（transient receptor potential vanilloid 1，TRPV1）对培养的血管平滑肌细胞（vascular smooth muscle cells，VSMCs）增殖的影响。方法用组织贴块法分别培养SHR和WKY大鼠的主动脉VSMCs，采用细胞免疫荧光进行鉴定。分别用辣椒素和iRTX激活和拮抗TRPV1受体，CCK-8法检测VSMCs增殖；Western blot法检测TRPV1、磷酸化-Akt（p-Akt）和总Akt（t-Akt）的蛋白表达。结果 ①SHR-VSMCs中TRPV1蛋白相对表达量低于WKY-VSMCs（0.32±0.05 vs 0.55±0.11， P0.05）；TRPV1激动剂辣椒素可显著上调SHR-VSMCs（0.65±0.19）和WKY-VSMCs(0.89±0.13)中TRPV1的表达(P0.05）。②SHR-VSMCs的增殖能力高于WKY-VSMCs（1.30±0.07 vs 0.88±0.23

P0.05）；辣椒素呈剂量依赖性地抑制SHR-VSMCs的增殖（对照组：1.30±0.07，1 μmol/L辣椒素组：0.93±0.10，10 μmol/L辣椒素组：0.83±0.16，P0.05）；应用iRTX拮抗TRPV1即拮抗辣椒素的抗增殖作用（1 μmol/L辣椒素组：0.93±0.10，1 μmol/L辣椒素+1 μmol/L iRTX组：1.23±0.14，P0.05）。③SHR-VSMCs中Akt磷酸化水平高于WKY-VSMCs（0.44±0.02 vs 0.29±0.09

P0.05）；辣椒素激活TRPV1抑制VSMCs中Akt的磷酸化（WKY-VSMCs：0.13±0.02

SHR-VSMCs: 0.23±0.03，P0.05）；TRPV1拮抗剂iRTX可拮抗辣椒素作用，使WKY-VSMCs（0.37±0.07）、SHR-VSMCs（0.43±0.10）中Akt磷酸化水平升高（P0.05）。结论激活TRPV1可能通过抑制Akt的磷酸化而抑制SHR-VSMCs增殖。

Abstract

Objective To determine the effect of transient receptor potential vanilloid 1 (TRPV1) on the proliferation of vascular smooth muscle cells (VSMCs) in spontaneously hypertensive rats (SHR). Methods VSMCs from aortas of SHR and corresponding age-matched Wistar Kyoto rats (WKY) were cultured using a tissue explant method

and identified by morphology and immunofluorescence assay. TRPV1 was activated by its agonist capsaicin and inhibited by its antagnosit 5’-iodo-resiniferatoxin (iRTX). Then

the proliferation of VSMCs was measured by CCK-8 assay. Western blotting was used to detect the expression of TRPV1

phosphorylated Akt (p-Akt) and total Akt. Results The expression of TRPV1 was lower in SHR-VSMCs(0.32±0.05) than in WKY-VSMCs（0.55±0.11

P0.05). TRPV1 agonist capsaicin increased the TRPV1 protein expression in WKY-VSMCs (0.65±0.198) and SHR-VSMCs (0.89±0.13

P0.05). SHR-VSMCs showed higher proliferative capability than WKY-VSMCs (1.30±0.07 vs 0.88±0.23

P0.05). TRPV1 agonist capsaicin inhibited the proliferation of SHR-VSMCs in a dose-dependent manner (control group: 1.30±0.07; 1 μmol/L capsaicin group: 0.93±0.10; 10 μmol/L capsaicin group: 0.83±0.16

P0.05)

which was counteracted by TRPV1 antagonist iRTX (1 μmol/L capsaicin group: 0.93±0.10; 1 μmol/L capsaicin + 1 μmol/L iRTX group: 1.23±0.14

P0.05). SHR-VSMCs showed increased expression of p-Akt in compared to WKY-VSMCs (0.44±0.02 vs 0.29±0.09

P0.05). Capsaicin reduced p-Akt expression in WKY-VSMCs (0.13±0.02) and SHR-VSMCs (0.23±0.03) (P0.05)

which was counteracted by TRPV1 antagonist iRTX (WKY: 0.37±0.07; SHR: 0.43±0.10) (P0.05). Conclusion Activation of TRPV1 suppresses the proliferation of VSMCs in SHR through down-regulating the expression of p-Akt.

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