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同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究

沈启睿 李永华 张文杰 王培

沈启睿, 李永华, 张文杰, 王培. 同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究[J]. 药学实践与服务, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
引用本文: 沈启睿, 李永华, 张文杰, 王培. 同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究[J]. 药学实践与服务, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
SHEN Qirui, LI Yonghua, ZHANG Wenjie, WANG Pei. Oxidative stress induced by homocysteine via activating JNK signaling pathway in vascular smooth muscle cells[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
Citation: SHEN Qirui, LI Yonghua, ZHANG Wenjie, WANG Pei. Oxidative stress induced by homocysteine via activating JNK signaling pathway in vascular smooth muscle cells[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005

同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究

doi: 10.3969/j.issn.1006-0111.2018.06.005
基金项目: 国家自然科学基金(81673485,81773719)

Oxidative stress induced by homocysteine via activating JNK signaling pathway in vascular smooth muscle cells

  • 摘要: 目的 观察同型半胱氨酸(Hcy)在A10血管平滑肌细胞株(vascular smooth muscle cells,VSMC)上对氧化应激的影响及其可能的分子机制。 方法 在体外培养的A10细胞上,用3个不同浓度(5、30和100 μmol/L)的Hcy孵育细胞共48 h,随后破裂细胞,一方面使用试剂盒检测细胞裂解液中的活性氧(ROS)水平、H2O2含量、总抗氧化能力(T-AOC),以评价其氧化应激情况。另一方面,用免疫印迹法检测磷酸化应激活化蛋白激酶(JNK)及总JNK的表达量。 结果 Hcy可诱导ROS、H2O2的含量升高,而导致T-AOC的水平下降。而且,Hcy增加了磷酸化JNK的蛋白表达量(P<0.05)。 结论 Hcy在VSMC上通过激活JNK信号通路诱导氧化应激。
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    [14] DALTON ML, GADSON PF, WRENN RW, et al. Homocysteine signal cascade:production of phospholipids, activation of protein kinase C, and the induction of c-fos and c-myb in smooth muscle cells[J]. FASEB J,1997,11(8):703-711.
    [15] BROWN JC, ROSENQUIST TH, MONAGHAn DT. ERK2 activation by homocysteine in vascular smooth muscle cells[J]. Biochem Biophys Res Commun,1998,251(3):669-676.
    [16] DORONZO G, RUSSO I, MATTIELLO L, et al. Homocysteine rapidly increases matrix metalloproteinase-2 expression and activity in cultured human vascular smooth muscle cells. Role of phosphatidyl inositol 3-kinase and mitogen activated protein kinase pathways[J]. Thromb Haemost,,2005,94(6):1285-1293.
    [17] CHANG L, XU JX, ZHAO J, et al. Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells[J]. Acta Pharmacol Sin,,2004,25(3):341-346.
    [18] SHIRPOOR A, SALAMI S, KHADEM ANSARI MH, et al. Ethanol promotes rat aortic vascular smooth muscle cell proliferation via increase of homocysteine and oxidized-low-density lipoprotein[J]. J Cardiol,2013,62(6):374-378.
    [19] LUO X, XIAO Y, SONG F, et al. Increased plasma S-adenosyl-homocysteine levels induce the proliferation and migration of VSMCs through an oxidative stress-ERK1/2 pathway in apoE(-/-) mice[J]. Cardiovasc Res,2012,95(2):241-250.
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  • 收稿日期:  2018-04-28
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同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究

doi: 10.3969/j.issn.1006-0111.2018.06.005
    基金项目:  国家自然科学基金(81673485,81773719)

摘要: 目的 观察同型半胱氨酸(Hcy)在A10血管平滑肌细胞株(vascular smooth muscle cells,VSMC)上对氧化应激的影响及其可能的分子机制。 方法 在体外培养的A10细胞上,用3个不同浓度(5、30和100 μmol/L)的Hcy孵育细胞共48 h,随后破裂细胞,一方面使用试剂盒检测细胞裂解液中的活性氧(ROS)水平、H2O2含量、总抗氧化能力(T-AOC),以评价其氧化应激情况。另一方面,用免疫印迹法检测磷酸化应激活化蛋白激酶(JNK)及总JNK的表达量。 结果 Hcy可诱导ROS、H2O2的含量升高,而导致T-AOC的水平下降。而且,Hcy增加了磷酸化JNK的蛋白表达量(P<0.05)。 结论 Hcy在VSMC上通过激活JNK信号通路诱导氧化应激。

English Abstract

沈启睿, 李永华, 张文杰, 王培. 同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究[J]. 药学实践与服务, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
引用本文: 沈启睿, 李永华, 张文杰, 王培. 同型半胱氨酸激活JNK信号通路诱导血管平滑肌细胞氧化应激的损伤研究[J]. 药学实践与服务, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
SHEN Qirui, LI Yonghua, ZHANG Wenjie, WANG Pei. Oxidative stress induced by homocysteine via activating JNK signaling pathway in vascular smooth muscle cells[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
Citation: SHEN Qirui, LI Yonghua, ZHANG Wenjie, WANG Pei. Oxidative stress induced by homocysteine via activating JNK signaling pathway in vascular smooth muscle cells[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(6): 499-502,511. doi: 10.3969/j.issn.1006-0111.2018.06.005
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