上海交通大学学报（医学版）

›› 2011, Vol. 31 ›› Issue (4): 392-.doi: 10.3969/j.issn.1674-8115.2011.04.002

• 论著（基础研究） • 上一篇    下一篇

蛋白激酶C不同亚型对丙泊酚血管舒张作用的影响

温翔宇1,2, 王 莉1, 崔永耀3, 江 伟1   

  1. 1.上海交通大学附属第六人民医院麻醉科, 上海200233； 2.苏州大学研究生部, 苏州 215006； 3.上海交通大学 基础医学院药理学教研室, 上海 200025
  • 出版日期:2011-04-28 发布日期:2011-04-28
  • 通讯作者: 王 莉, 电子信箱: liwang1118@hotmail.com。
  • 作者简介:温翔宇（1983—）, 女, 硕士生；电子信箱: wxyzhjh@126.com。
  • 基金资助:

    国家自然科学基金（30972842）；上海市自然科学基金（09ZR1424000)

Effects of different protein kinase C isoforms on vasodilation induced by propofol

WEN Xiang-yu1,2, WANG Li1, CUI Yong-yao3, JIANG Wei1   

  1. 1.Department of Anesthesiology, The Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233, China；2.Department Postgraduate, Soochow University, Suzhou 215006, China；3.Department of Pharmacology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2011-04-28 Published:2011-04-28
  • Supported by:

    National Natural Science Foundation of China, 30972842；Shanghai Municipal Natural Science Foundation, 09ZR1424000

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摘要：

目的 探讨丙泊酚的血管舒张作用与蛋白激酶C （PKC）不同亚型间的关系。方法 将SD大鼠胸主动脉环随机分为内皮完整组（n=36）和去内皮组（n=36），每组各分6个亚组：①10 nmol/L Go6976+1×10-6 mol/L去甲肾上腺素（NA）+丙泊酚处理组（n=6）；②10 μmol/L Rottlerin+1×10-6 mol/L NA+丙泊酚处理组（n=6）；③2 μmol/L PKCε-Pseudo（假底物）+1×10-6 mol/L NA+丙泊酚处理组（n=6）；④2 μmol/L PKCθ-Pseudo+1×10-6 mol/L NA+丙泊酚处理组（n=6）；⑤2 μmol/L PKCζ-Pseudo+1×10-6 mol/L NA+丙泊酚处理组（n=6）；⑥1×10-6 mol/L NA+丙泊酚处理组（对照组，n=6）。PKCα抑制剂Go6976，PKCδ抑制剂Rottlerin，PKCζ、θ和ε假底物孵育血管环30 min后，加1×10-6 mol/L NA收缩血管环达峰值，每15 min加递增浓度的丙泊酚（1×10-6、5×10-6、1×10-5、5×10-5、1×10-4 mol/L），观察血管张力的变化。结果 内皮完整时，Go6976、PKCε假底物和PKCθ假底物减小丙泊酚引起的血管舒张幅度，与内皮完整的对照组相比差异有统计学意义（P<0.05）； Rottlerin抑制丙泊酚的血管舒张效应，且在1×10-6~5×10-5 mol/L丙泊酚作用时将舒张效应转为收缩（P<0.05）。去内皮时，Rottlerin、PKCε假底物和PKCθ假底物分别增大相同浓度丙泊酚作用下的血管舒张幅度，与去内皮对照组相比差异有统计学意义（P<0.05）；Go6976和PKCζ假底物分别增大1×10-5~1×10-4 mol/L丙泊酚作用下的血管舒张幅度（P<0.05）。结论 PKCα、δ、ε、θ参与了内皮完整时丙泊酚引起的血管舒张。

关键词: 丙泊酚, 胸主动脉, 血管舒张, 蛋白激酶C

Abstract:

Objective To investigate the relationship between propofol-induced vasodilation and different protein kinase C(PKC) isoforms. Methods Vascular rings of SD rats were randomly divided into endothelium-intact group (n=36) and endothelium-denuded group (n=36), and each group was divided into 6 subgroups: ①10 nmol/L Go6976+1×10-6 mol/L norepinephrine (NA)+ propofol group (n=6)；②10 μmol/L Rottlerin+1×10-6 mol/L NA+propofol group （n=6）；③ 2 μmol/L PKCε-Pseudo+1×10-6 mol/L NA+ propofol group （n=6）；④2 μmol/L PKCθ-Pseudo+1×10-6 mol/L NA+ propofol group（n=6）；⑤2 μmol/L PKCζ-Pseudo+1×10-6 mol/L NA+ propofol group （n=6）；⑥1×10-6 mol/L NA+ propofol group(control group, n=6). PKCα inhibitor Go6976, PKCδ inhibitor Rottlerin, PKCζ-Pseudo, PKCθ-Pseudo and PKCε-Pseudo were used to pretreat isolated thoracic aorta rings for 30 min. Then 1×10-6 mol/L NA evoked a steady maximal vasoconstriction, propofol was added in progressively increasing cumulative concentrations at a 15 min interval (1×10-6, 5×10-6, 1×10-5, 5×10-5 and 1×10-4 mol/L), and the changes of vascular tone were observed. Results In endothelium-intact group, compared with endothelium-intact group, Go6976, PKCε-Pseudo and PKCθ-Pseudo inhibited propofol-induced vasodilation （P<0.05). Rottlerin also inhibited propofol-induced vasodilation, and even reversed the effect (1×10-6 to 5×10-5 mol/L propofol)(P<0.05). In endothelium-denuded group, compared with endotheliumdenuded control group, Rottlerin, PKCθ-Pseudo and PKCε-Pseudo enhanced propofol-induced vasodilation (P<0.05), and Go6976 and PKCζ-Pseudo enhanced vasodilation induced by 1×10-5 to 1×10-4 mol/L propofol (P<0.05). Conclusion PKCα, PKCδ, PKCε and PKCθ involve in propofol-induced vasodilation in intact endothelium.

Key words: propofol, thoracic aorta, vasodilatation, protein kinase C