中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (20): 3686-3690.doi: 10.3969/j.issn.1673-8225.2010.20.018

• 组织构建与中医药 tissue construction and traditional Chinese medicine • 上一篇    下一篇

电针干预自发性高血压大鼠主动脉丝裂原活化蛋白激酶磷酸酶1及磷酸化细胞外信号调节激酶1/2蛋白的表达

蒋 璘1，2，何 可2，陈楚淘2，张 泓2   

  1. 1长沙民政职业技术学院，湖南省长沙市  410004； 
    2湖南中医药大学，湖南省长沙市410208
  • 出版日期:2010-05-14 发布日期:2010-05-14
  • 通讯作者: 张 泓，教授，博士，硕士研究生导师，湖南中医药大学，湖南省长沙市 410208 zh5381271@sina.com
  • 作者简介:蒋 璘，女，1976年生，湖南省邵阳市人，汉族，湖南中医药大学在读硕士，讲师，主要从事针灸治病机理研究。 149765923@qq.com
  • 基金资助:

    湖南省科技厅自然科学基金委员会项目(03JJY4026)、湖南省中医药管理局资助项目(202004)、国家自然科学基金青年科学基金项目(30901901)。

Electroacupuncture intervention on the expression of mitogen activated protein kinase phosphatase-1 and phosphorylated extracellular signal-regulated kinase 1/2 in aorta of rats with spontaneous hypertension

Jiang Lin1,2, He Ke2, Chen Chu-tao2, Zhang Hong2   

  1. 1Changsha Social Work College, Changsha  410004, Hunan Province, China;
    2Hunan University of Chinese Medicine, Changsha  410208, Hunan Province, China 
  • Online:2010-05-14 Published:2010-05-14
  • Contact: Zhang Hong, Professor, Doctor, Master’s supervisor, Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China zh5381271@sina.com
  • About author:Jiang Lin, Studying for master’s degree, Lecturer, Changsha Social Work College, Changsha 410004, Hunan Province, China; Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China 149765923@qq.com
  • Supported by:

    the Natural Science Commission of Hunan Provincial Science and Techonology Department, No. 03JJY4026*;
    Administration of Traditional Chinese Medicine of Hunan Province, No. 202004*;
    National Natural Science Funds for Distinguished Young Scholars, No. 30901901*

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被引次数

24

摘要：

背景：近年来大量临床研究表明针刺风池、太冲、曲池等穴位能有效降低血压，可用于高血压，但对其治疗的分子机制尚未阐明。

目的：观察针刺大鼠风池、太冲、曲池等穴位对丝裂原活化蛋白激酶信号转导调控系统的影响，从而探讨针刺治疗高血压的分子机制。

方法：选取8月龄自发性高血压雄性Wistar大鼠14只，随机分为针刺组和模型组，每组7只；另选取同月龄正常血压雄性Wistar-Kyoto大鼠7只作为对照组。对针刺组大鼠采用电针针刺双侧风池、曲池和三阴交穴，毫针刺太溪和太冲穴。3周后采用RT-PCR方法检测各组大鼠主动脉组织丝裂原活化蛋白激酶磷酸酶1 mRAN的表达，Western blot方法检测丝裂原活化蛋白激酶磷酸酶1、磷酸化细胞外信号调节激酶1/2蛋白表达。

结果与结论：与对照组比较，模型组主动脉组织磷酸化细胞外信号调节激酶1/2蛋白表达水平升高，丝裂原活化蛋白激酶磷酸酶1 mRNA及其蛋白表达水平降低(P < 0.01)；与模型组比较，针刺组主动脉组织磷酸化细胞外信号调节激酶1/2蛋白表达水平降低，丝裂原活化蛋白激酶磷酸酶1 mRNA及其蛋白表达水平升高(P < 0.05)。提示针刺治疗自发性高血压大鼠可能是通过调控丝裂原活化蛋白激酶信号转导途径，增强磷酸化细胞外信号调节激酶1/2蛋白表达，降低丝裂原活化蛋白激酶磷酸酶1蛋白表达，从而改善血管重塑，降低血压。

关键词: 电针, 自发性高血压大鼠, 主动脉, 丝裂原活化蛋白激酶磷酸酶1, 磷酸化细胞外信号调节激酶1/2蛋白, 高血压

Abstract:

BACKGROUND: In recent years, a large number of clinical studies have shown that acupuncture Fengchi (GB 20), Taichong  (LR 3), Quchi (LI 11) points can effectively lower blood pressure, which can be used for the treatment of hypertension, but the molecular mechanism of this treatment has not been clarified.

OBJECTIVE: To explore the molecular mechanism of acupuncture treatment of hypertension via observing the effects of acupuncture Fengchi (GB 20), Taichong (LR 3), Quchi (LI 11) points on the mitogen-activated protein kinase (MAPK) signal transduction system.

METHODS: A total of 14 8-month male spontaneously hypertensive rats were randomly divided into the acupuncture and model groups, with 7 animals in each group. Additional 7 male Wistar-Kyoto rats were served as the control group. Rats in the acupuncture group received electroacupuncture at bilateral Fengchi (GB 20), Quchi (LI 11), and Sanyinjiao (SP 6) points, pin acupuncture at the Taixi (KI 3) and Taichong (LR 3) points. The expression of MAPK phosphatase-1 (MKP-1) mRNA, MKP-1 protein and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) in aorta was detected by RT-PCR and Western blot at 3 weeks after operation.

RESULTS AND CONCLUSION: Compared with the control group, the p-ERK1/2 level was increased and the MKP-1 mRNA and protein levels were decreased in the model group (P < 0.05). Compared with the model group, the p-ERK1/2 level was decreased and the MKP-1 mRNA and protein levels were increased in the acupuncture group (P < 0.05). The results revealed that acupuncture treatment of spontaneously hypertensive rats may be through regulation of MAPK signal transduction pathway to enhance p-ERK1/2 protein expression and reduce MKP-1 protein expression, thereby, improve vascular remodeling and decrease blood pressure.

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