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| M3受体通过激活MEK1/2-ERK1/2信号通路促进H9c2心肌细胞生存 | |
| 引用本文： | 张伟志,黄灿,杨一峰. M3受体通过激活MEK1/2-ERK1/2信号通路促进H9c2心肌细胞生存[J]. 中南药学, 2011, 9(3): 161-165. DOI: 10.3969/j.issn.1672-2981.2011.03.001 |
| 作者姓名： | 张伟志 黄灿 杨一峰 |
| 作者单位： | 中南大学湘雅二医院小儿心脏外科,长沙,410011 |
| 摘 要： | 目的研究毒蕈碱型胆碱受体(M受体)对H9c2心肌细胞MEK1/2-ERK1/2信号通路的调控作用及其对细胞活力的影响。方法 H9c2心肌细胞用非选择性或选择性M受体拮抗药处理30 min之后,以氨甲酰胆碱刺激细胞,然后用Western Blot检测全细胞蛋白质中MEK1/2和ERK1/2磷酸化水平的变化,采用Alamar Blue法检测细胞活力。结果以氨甲酰胆碱刺激H9c2心肌细胞能显著增加MEK1/2和ERK1/2的磷酸化水平,这种活化作用可被非选择性M受体拮抗药阿托品完全阻断;M3受体选择性拮抗药DAU 5884可以阻断氨甲酰胆碱对MEK1/2-ERK1/2的激活,但M1、M2和M4受体的选择性拮抗药则没有这种阻断作用;在无血清的培养基中,氨甲酰胆碱能增加H9c2心肌细胞的生存能力,这种细胞保护作用可被阿托品和DAU 5884消除。结论在H9c2心肌细胞中,氨甲酰胆碱通过M3受体调控MEK1/2-ERK1/2信号通路,并由此促进细胞的生存。 |
| 关 键 词： | 毒蕈碱型胆碱受体 MEK1/2-ERK1/2信号通路 H9c2心肌细胞 细胞生存 |
M3 muscarinic acetylcholine receptors promote the survival of H9c2 cardiomyocytes through activating MEK1/2-ERKl/2 signaling pathway |
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| ZHANG Wei-zhi,HUANG Can,YANG Yi-feng. M3 muscarinic acetylcholine receptors promote the survival of H9c2 cardiomyocytes through activating MEK1/2-ERKl/2 signaling pathway[J]. Central South Pharmacy, 2011, 9(3): 161-165. DOI: 10.3969/j.issn.1672-2981.2011.03.001 | |
| Authors: | ZHANG Wei-zhi HUANG Can YANG Yi-feng |
| Affiliation: | ZHANG Wei-zhi,HUANG Can,YANG Yi-feng*(Department of Pediatric Cardiac Surgery,Second Xiangya Hospital,Central South University,Changsha 410011) |
| Abstract: | Objective To determine the effect of muscarinic acetylcholine receptor(M-receptor) stimulation on the activation of MEK1/2-ERK1/2 signaling pathway and the cell viability in H9c2 cardiomyocytes.Methods H9c2 cardiomyocytes were treated with or without non-selective or subtype selective M-receptor antagonists,then treated with carbachol or vehicle.The cell lysates were subjected to Western Blot to determine the phosphorylation level of MEK1/2 and ERK1/2.Alarma Blue assays were employed to measure the cell via... |
| Keywords: | muscarinic acetylcholine receptor MEK1/2-ERK1/2 signaling pathway H9c2 cardiomyocyte cell survival |
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