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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

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文章导航 > 药学实践与服务  > 2018 >  36(6): 499-502,511
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
shu
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
shu

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
  • 1.

    中国计量大学生命科学院动植物检疫系, 浙江 杭州 310018

  • 2.

    第二军医大学附属长征医院麻醉科, 上海 200003

  • 3.

    第二军医大学药学院药理学教研室, 上海 200433

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

  • 1.

    School of Life Sciences, China Jiliang University, Hangzhou 310018, China

  • 2.

    Department of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, Shanghai 200003, China

  • 3.

    Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

  • 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。
    Abstract: Objective To investigate the influence and the underlying mechanisms of homocysteine on oxidative stress production in vascular smooth muscle cells (VSMC). Methods A10 cell line (a kind of VSMC) was cultured in vitro. Three different concentrations of homocysteine (5, 30 and 100 μmol/L) were added into the medium for 48 hours and then cells were lysed for determination of reactive oxygen species (ROS) production, H2O2 level and total anti-oxidant capacity. Moreover, the effects of homocysteine on JNK signaling pathway were evaluated by immunoblotting. Results ROS production (P<0.05) in VSMC were induced by three different concentrations of homocysteine (5, 30 and 100 μmol/L). Two concentrations of homocysteine (30 and 100 μmol/L) increased H2O2 content and decreased T-AOC. Moreover, homocysteine induced phosphorylation of JNK in VSMC in a dose-dependent manner (P<0.05). Conclusion Oxidative stress induced by homocysteine via activating JNK signaling pathway in VSMC.
  • [1] NYGARD O, VOLLSET SE, REFSUM H, et al. Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study[J]. JAMA,1995,274(19):1526-1533.
    [2] LI Z, SUN L, ZHANG H, et al. Elevated plasma homocysteine was associated with hemorrhagic and ischemic stroke, but methylenetetrahydrofolate reductase gene C677T polymorphism was a risk factor for thrombotic stroke:a multicenter case-control study in China[J]. Stroke,2003,34(9):2085-2090.
    [3] YE Z, WANG C, ZHANG Q, et al. Prevalence of homocysteine-related hypertension in patients with chronic kidney disease[J]. J Clin Hypertens (Greenwich),2017,19(2):151-160.
    [4] HAN L, WU Q, WANG C, et al. Homocysteine, ischemic stroke, and coronary heart disease in hypertensive patients:a population-based, prospective cohort study[J]. Stroke,2015,46(7):1777-1786.
    [5] RODRIGO R, PASSALACQUA W, ARAYA J, et al. Implications of oxidative stress and homocysteine in the pathophysiology of essential hypertension[J]. J Cardiovasc Pharmacol,2003,42(4):453-461.
    [6] XI H, ZHANG Y, XU Y, et al. Caspase-1 inflammasome activation mediates homocysteine-induced pyrop-apoptosis in endothelial cells[J]. Circ Res,2016,118(10):1525-1539.
    [7] CHANG PY, LU SC, LEE CM, et al. Homocysteine inhibits arterial endothelial cell growth through transcriptional downregulation of fibroblast growth factor-2 involving G protein and DNA methylation[J]. Circ Res,2008,102(8):933-941.
    [8] ZHANG D, XIE X, CHEN Y, et al. Homocysteine upregulates soluble epoxide hydrolase in vascular endothelium in vitro and in vivo[J]. Circ Res,2012,110(6):808-817.
    [9] MUJUMDAR VS, HAYDEN MR, TYAGI SC. Homocyst(e)ine induces calcium second messenger in vascular smooth muscle cells[J]. J Cell Physiol,2000,183(1):28-36.
    [10] ZHANG D, CHEN Y, XIE X, et al. Homocysteine activates vascular smooth muscle cells by DNA demethylation of platelet-derived growth factor in endothelial cells[J]. J Mol Cell Cardiol,2012,53(4):487-496.
    [11] ZOU T, YANG W, HOU Z, et al. Homocysteine enhances cell proliferation in vascular smooth muscle cells:role of p38 MAPK and p47phox[J]. Acta Biochim Biophys Sin (Shanghai),2010,42(12):908-915.
    [12] TSAI JC, WANG H, PERRELLA MA, et al. Induction of cyclin A gene expression by homocysteine in vascular smooth muscle cells[J]. J Clin Invest,1996,97(1):146-153.
    [13] TSAI JC, PERRELLA MA, YOSHIZUMI M, et al. Promotion of vascular smooth muscle cell growth by homocysteine:a link to atherosclerosis[J]. Proc Natl Acad Sci USA,1994,91(14):6369-6373.
    [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.
    [20] ZHANG L, ZHOU M, WANG Y, et al. miR-92a inhibits vascular smooth muscle cell apoptosis:role of the MKK4-JNK pathway[J]. Apoptosis,2014,19(6):975-983.
    [21] LIU YZ, CHEN JK, LI ZP, et al. High-salt diet enhances hippocampal oxidative stress and cognitive impairment in mice[J]. Neurobiol Learn Mem,2014,114:10-15.
    [22] ZHANG XJ, HE C, TIAN K, et al. Ginsenoside Rb1 attenuates angiotensin Ⅱ-induced abdominal aortic aneurysm through inactivation of the JNK and p38 signaling pathways[J]. Vascul Pharmacol,2015,73:86-95.
    [23] CHENG Y, QIU F, TASHIRO S, et al. ERK and JNK mediate TNFalpha-induced p53 activation in apoptotic and autophagic L929 cell death[J]. Biochem Biophys Res Commun,2008,376(3):483-488.
    [24] SHEN HM, LIU ZG. JNK signaling pathway is a key modulator in cell death mediated by reactive oxygen and nitrogen species[J]. Free Radic Biol Med,2006,40(6):928-939.
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  • 收稿日期:  2018-04-28
  • 修回日期:  2018-06-01

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
  • 1. 中国计量大学生命科学院动植物检疫系, 浙江 杭州 310018
  • 2. 第二军医大学附属长征医院麻醉科, 上海 200003
  • 3. 第二军医大学药学院药理学教研室, 上海 200433
    • 基金项目:  国家自然科学基金（81673485，81773719）
  • 收稿日期: 2018-04-28
  • 修回日期: 2018-06-01

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
shu
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
shu

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