欢迎访问《中国临床药理学与治疗学》杂志官方网站,今天是

中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (1): 65-68.

• 研究原著 • 上一篇    下一篇

Ca2+/CaM-CaN 途径参与神经肽Y 诱导的大鼠心肌细胞肥大

董颀, 陈敏生1, 李晓云1, 黄少华2, 李荧辉3, 张舒4, 刘振秀3   

  1. 广州医学院生理教研室, 1第二附属医院心血管内科, 2学报编辑部, 广州 510182, 广东;
    3航天医学工程研究所, 北京 100094;
    4第四军医大学航空生理系, 西安 710054, 陕西
  • 收稿日期:2004-11-09 修回日期:2004-12-24 出版日期:2005-01-26 发布日期:2020-11-19
  • 通讯作者: 陈敏生, 男, 硕士, 教授, 博士生导师, 从事心血管疾病研究。Tel:020-81340199 E-mail:gzminsheng@vip.163.com
  • 作者简介:董颀, 女, 硕士, 助理研究员。Tel:020-81340199 E-mail:dongqistar@hotmail.com
  • 基金资助:
    广东省自然科学基金资助项目(No980466)

Effects of Ca2+ CaM-dependent calcineurin signaling pathway on cardiomyocytes hypertrophy of rats induced by neuropeptide Y

DONG Qi, CHEN Min-sheng1, HUANG Shao-hua2, LI Xiao-yun1, LI Ying-hui3, ZHANG Shu4, LIU Zhen-xiu3   

  1. Department of Physiology, 1Department of Cardiology, the Second Affiliated Hospital, 2Editory of Academic Journal, Guangzhou Medical College, Guangzhou 510260, Guangdong, China;
    3Institute of Spaceflight Medical engine, Beijng 100094;
    4Department of Spaceflight Physiology, the Forth Military Medical University, Xi'an 710054, Shannxi
  • Received:2004-11-09 Revised:2004-12-24 Online:2005-01-26 Published:2020-11-19

摘要: 目的: 探讨Ca2+ CaM 依赖的钙调神经磷酸酶(CaN) 途径在神经肽Y(NPY) 诱导心肌细胞肥大中的作用。方法: 用NPY (10、100 nmol·L-1) 刺激WISTAR 乳鼠心肌细胞, 并用CaN 特异性抑制剂环胞霉素A 加以干预。应用3H-Leu 掺入法测定心肌细胞蛋白质合成速率, 用免疫印迹(Western-blot) 和组织化学法分别测定心肌细胞内CaN-α蛋白表达和CaN 酶的活性。结果: 较高浓度NPY(100 nmol·L-1) 可明显增加心肌细胞3H-Leu 掺入量(P < 0.05), 加入CsA 可阻断上述效应;NPY(100 nmol·L-1) 还可明显增加心肌细胞内CaN 酶比活性(P <0.05), 并刺激心肌细胞CaN-α蛋白表达(P <0.05) 。结论: NPY 可活化大鼠心肌细胞Ca2+CaM-CaN 途径, 而CaN 特异性抑制剂环胞霉素A 可抑制NPY 诱导的心肌肥大, 说明Ca2+ CaM 依赖的钙调神经磷酸酶(CaN) 途径参与神经肽Y 诱导的心肌细胞肥大效应。

关键词: 神经肽Y, 钙调神经磷酸酶, 胞霉素A, 心肌细胞肥大

Abstract: AIM: To investigate the effects of Ca2+ CaM-dependent calcineurin (CaN) signaling pathway on cardiomyocytes hypertrophy of rat induced by neuropeptide Y (NPY).METHODS: Cardiomyocytes of neonatal Wistar rats were cultured with NPY of various concentrations (10, 100 nmol·L-1).Cyclosporine A (CsA) was used to inhibit the activity of CaN.The methods of 3H-Leu incorporation was used to assess protein synthesis rate in cardiomyocytes.Western-blot and histochemistry were used to measure CaN protein expression and CaN activity in cardiomyocytes.RESULTS: 3H-Leu incorporation of cardiomyocytes were increased significantly by 100 nmol·L-1NPY (P <0.05) and decreased by CsA.CaN activity and CaN-αprotein expression was elevated markedly in cardiomyocytes by 100 nmol·L-1NPY (P < 0.05).CONCLUSION: Neuropeptide Y activates Ca2+ CaM-dependent calcineurin signal pathway, and CsA can inhibit cardiomyocytes hypertrophy induced by NPY. It indicates that Ca2+ CaM-dependent calcineurin (CaN) signaling pathway plays an important role in cardiomyocytes hypertrophy of rats induced by NPY.

Key words: neuropeptide Y, calcineurin, cardiomyocytes hypertrophy

中图分类号: