| 冯念苹 林静涵 聂雪丹 孙丽娜 张黎明 梁庆成 王正非 郑海洪.Ca2+转运通路对金雀异黄酮舒张大鼠脑血管作用的影响[J].现代生物医学进展英文版,2015,15(19):3645-3650. |
| Ca2+转运通路对金雀异黄酮舒张大鼠脑血管作用的影响 |
| Role of Ca2+ Transport Pathways in the Effects of Genistein onSerotonin-Activated Cerebrovascular Contraction |
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| DOI： |
| 中文关键词: Ca2+运输 金雀异黄酮 5 -羟色胺 脑血管收缩 |
| 英文关键词: Ca2+ transport pathways Genistein Serotonin Cerebrovascular contraction |
| 基金项目:黑龙江省教育厅科学技术研究项目(12521336) |
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| 中文摘要: |
| 目的：研究Ca2+转运通路对金雀异黄酮舒张大鼠脑血管作用的影响。方法：75只大鼠被随机分为3 组，分别经由二甲亚砜、
金雀异黄酮和酪氨酸磷酸化抑制剂A47 处理基底动脉及Willis 环血管。每组大鼠进一步划分成5 个亚组，每个亚组用不同浓度
的细胞外Ca2+处理，分为:0、0.6、1.2、1.8 和3.6 mMCa2+组。5- 羟色胺诱导血管收缩。测定大鼠基底动脉管壁厚度与官腔周长的比
值；荧光成像分析法测定血管平滑肌细胞细胞内Ca2+浓度；免疫印迹分析检测肌球蛋白轻链激酶(MLCK)，蛋白质磷酸酶催化亚
基1(PP1)，肌凝蛋白磷酸酶目标亚基1(MYPT1)的表达来测定血管平滑肌细胞Ca2+敏感性。结果：金雀异黄酮和酪氨酸磷酸化抑
制剂A47 显著降低大鼠基底动脉管壁厚度与官腔周长的比值（P＜0.01），Ca2+内流（P＜0.01，P＜0.05）及MLCK 的表达（P＜
0.01）；增加PP1 和MYPT1 的表达（P＜0.01）。细胞外Ca2+与金雀异黄酮及酪氨酸磷酸化抑制剂A47有协同效应。硝苯地平和毒
胡萝卜素可废除该效应。结论：低细胞外Ca2+水平增强了金雀异黄酮和酪氨酸磷酸化抑制剂A47 的血管舒张作用。L型电压门控
Ca2+通道(L-VGCC)和肌浆网Ca2+库(SR)参与交互效应。 |
| 英文摘要: |
| Objective:To study the role of Ca2+ transport pathways in the effects of genistein on serotonin activated
cerebrovascular contraction.Methods:Seventy five rats were randomly divided into 3 groups. Basilar artery (BA) and Willis ring in
different groups were incubated with dimethyl sulfoxide, genistein and tyrphostin A47 (Tyr A47).Each group was further divided into
subgroups of 5 rats that were treated with different concentrations of 0, 0.6, 1.2, 1.8 and 3.6 mM Ca2+. Serotonin induced
vasoconstriction. The effects of genistein Tyr A47 on serotonin-activated contraction were examined by measuring the ratio of tube wall
thickness and the lumen perimeter of the BA. Intracellular Ca2+ concentration ([Ca2+]i) of vascular smooth muscle cells was determined by
ratiometric fluorescence imaging analysis. The Ca2+ sensitivity was determined by measuring the expression of myosin light chain kinase
(MLCK), protein phosphatase catalytic submit1 (PP1) and myosin phosphatase target submit1 (MYPT1) by Western blot analysis.Results:Genistein and Tyr A47 significantly reduced the ratio of tube wall thickness and the lumen perimeter of BA（P＜0.01）, [Ca2+]i
（P ＜0.01，P＜0.05）and the expression of MLCK （P ＜0.01）. Opposite results were observed for PP1 and MYPT1 （P ＜0.01）.
Extracellular Ca2+ had a synergistic effect on genistein and Tyr A47. The effect was abolished by nifedipine and thapsigargin.Conclusion:Low extracellular Ca2+ enhanced the vasodilatation that was stimulated by genistein and Tyr A47. L-type voltage-gated Ca2+
channel (L-VGCC) and sarcoplasmic reticulum(SR) Ca2+were involved in the interaction. |
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