| 引用本文: | 杨光明，徐竞，李涛，明佳，陈玮，刘良明.蛋白激酶C ε亚型在AVP调节休克血管MLC20磷酸化水平及MLCK/MLCP活性中的作用[J].中国现代应用药学,2009,(9):712-715. |
| YANG Guangming, XU Jing, LI Tao, MING Jia, CHEN wei, LIU Liangming.Effect of PKC ε Isoform in AVP Regulating the MLC20 Phosphorylation of SMA After Shock and MLCP/MLCK Activity of VSMC[J].Chin J Mod Appl Pharm(中国现代应用药学),2009,(9):712-715. |
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| 摘要: |
| 目的 研究蛋白激酶C(PKC) ε亚型在精氨酸血管加压素(AVP)调节休克血管肌球蛋白轻链(MLC20)磷酸化及缺氧血管平滑肌细胞(VSMC)肌球蛋白轻链激酶(MLCK)和肌球蛋白轻链磷酸酶(MLCP)活性中的作用。方法 采用大鼠失血性休克模型和缺氧培养VSMC，观察PKC ε亚型在AVP调节失血性休克大鼠肠系膜上动脉(SMA)血管平滑肌MLC20磷酸化水平中的作用，同时检测缺氧VSMC中MLCK和MLCP活性的变化。结果 失血性休克后SMA血管平滑肌MLC20磷酸化水平降低，同时缺氧VSMC的MLCP活性明显升高，MLCK活性明显降低；AVP处理可显著升高MLC20磷酸化水平和抑制缺氧VSMC的MLCP活性升高，特异性的PKC ε抑制肽可明显拮抗AVP升高MLC20磷酸化、降低MLCP的作用；而AVP和PKC ε抑制肽对MLCK活性的变化无明显影响。结论 AVP可通过PKC ε亚型来发挥改善休克血管反应性的作用，其机制可能是通过抑制MLCP活性、升高MLC20磷酸化水平，进而增强血管平滑肌细胞钙敏感性升高血管反应性。 |
| 关键词: 失血性休克 缺氧 血管平滑肌细胞 蛋白激酶C ε亚型 精氨酸血管加压素 |
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| Effect of PKC ε Isoform in AVP Regulating the MLC20 Phosphorylation of SMA After Shock and MLCP/MLCK Activity of VSMC |
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YANG Guangming, XU Jing, LI Tao, MING Jia, CHEN wei, LIU Liangming
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| Abstract: |
| OBJECTIVE The present study was aimed to investigate the roles of protein kinase C (PKC) ε isoform in the regulation of arginine vasopressin (AVP) on myosin light chain (MLC20) phosphorylation of vascular smooth muscle after shock, and myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK) activity of vascular smooth muscle cell (VSMC) after hypoxia. METHODS With hemorrhagic shock model from rats and hypoxia-treated VSMC，the effects of PKC ε isoform in AVP regulating the phosphorylation of MLC20 of superior mesenteric artery (SMA) after shock, and the activity of MLCP/MLCK in VSMC were observed. RESULTS The MLC20 phosphorylation of SMA following hemorrhagic shock was significantly decreased, and at the same time, the MLCP activity of VSMC was significantly increased after hypoxia, with a decrease in MLCK activity. AVP treatment resulted in an increase in MLC20 phosphorylation of SMA and decreased in MLCP activity of VSMC, which could be inhibited by PKC ε isoform inhibitory peptide. AVP and PKC ε isoform inhibitory peptide had no significant influence on MLCK activity. CONCLUSION AVP can restore the decreased vascular reactivity after hemorrhagic shock via PKC ε isoform, and its mechanisms is possibly through inhibiting the activity of MLCP and increasing MLC20 phosphorylation, followed by improves the calcium sensitivity of VSMC and enhances the vascular reactivity. |
| Key words: hemorrhagic shock hypoxia vascular smooth muscle cell protein kinase C ε isoform arginine vasopressin |
