留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码
x 关闭 永久关闭

应中央军委要求，2022年9月起，《药学实践杂志》将更名为《药学实践与服务》，双月刊，正文96页；2023年1月起，拟出版月刊，正文64页，数据库收录情况与原《药学实践杂志》相同。欢迎作者踊跃投稿！

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

downloadPDF
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.
  • [1] 陈金涛, 乔子婴, 章祎俊, 许玲, 郑月娟, 何宗阳, 刘良善, 马明华, 张若曦, 王振伟, 年华.  基于网络药理学、分子对接研究金芪清疏颗粒治疗CAP的潜在机制 . 药学实践与服务, 2024, 42(): 1-9. doi: 10.12206/j.issn.2097-2024.202312014
    [2] 武菲菲, 张绡绮, 连敬, 杨晶, 翟蒙恩, 乔锐, 徐臣年, 杨婷婷.  黄芪甲苷激活ROCK/JNK介导自噬减轻异丙肾上腺素诱导的小鼠心肌纤维化 . 药学实践与服务, 2023, 41(8): 478-484. doi: 10.12206/j.issn.2097-2024.202212056
    [3] 王道鑫, 张添光, 缪朝玉.  血管内皮细胞线粒体氧化应激与动脉粥样硬化 . 药学实践与服务, 2023, 41(6): 329-334, 392. doi: 10.12206/j.issn.2097-2024.202205116
    [4] 石志群, 高迎春, 张冬梅, 陈克明, 景临林, 马慧萍.  7-羟乙基白杨素对高原脑水肿的作用机制初探 . 药学实践与服务, 2022, 40(5): 399-402, 415. doi: 10.12206/j.issn.2097-2024.202205090
    [5] 钱珺, 谢凡, 卫克昭, 高建平, 李文艳.  复方滋阴颗粒对去卵巢大鼠性激素和氧化应激水平的影响 . 药学实践与服务, 2020, 38(5): 431-434. doi: 10.12206/j.issn.1006-0111.201912023
    [6] 刘景雪, 黄瑾.  改善糖尿病内皮祖细胞功能的研究进展 . 药学实践与服务, 2020, 38(1): 18-21. doi: 10.3969/j.issn.1006-0111.201906065
    [7] 陈静, 陈明珠, 黄玉香, 程晶, 黄雅平.  绿萼梅总黄酮对慢性温和刺激所致抑郁大鼠神经内分泌和氧化应激的影响 . 药学实践与服务, 2019, 37(3): 226-230. doi: 10.3969/j.issn.1006-0111.2019.03.007
    [8] 张莉燕, 宋金春.  “质量源于设计”在制备N-乙酰半胱氨酸注射液中的应用 . 药学实践与服务, 2019, 37(6): 552-558. doi: 10.3969/j.issn.1006-0111.2019.06.016
    [9] 朱玉婷, 王谨慧, 李茂星, 李晓琳, 陶文迪, 刘延彤.  毛蕊花苷对高原缺氧小鼠记忆损伤的改善及机制研究 . 药学实践与服务, 2019, 37(1): 23-26. doi: 10.3969/j.issn.1006-0111.2019.01.006
    [10] 赵安鹏, 靳婷, 王荣.  槟榔醇提物对H9C2心肌细胞的抗缺氧保护作用 . 药学实践与服务, 2019, 37(4): 294-298. doi: 10.3969/j.issn.1006-0111.2019.04.002
    [11] 武柠子, 马慧萍, 王昕, 何蕾, 景临林, 贾正平.  模拟高原缺氧环境对大鼠心、脑组织损伤的研究 . 药学实践与服务, 2018, 36(3): 250-254. doi: 10.3969/j.issn.1006-0111.2018.03.013
    [12] 谢华, 王延玲, 王昌, 李文斌, 贾正平, 王荣.  美托洛尔对急进海拔3400 m大鼠的心肌保护作用研究 . 药学实践与服务, 2018, 36(3): 238-242. doi: 10.3969/j.issn.1006-0111.2018.03.010
    [13] 张金宇, 王丽红, 秦玉璘, 张璐璐, 姜远英, 曹永兵.  转录因子Cup2对白念珠菌铜离子代谢、氧化应激调控作用的初步研究 . 药学实践与服务, 2017, 35(3): 224-228. doi: 10.3969/j.issn.1006-0111.2017.03.008
    [14] 沈玲玲, 应茵, 陆绪亮, 宋洪涛, 戴海斌.  长期丙戊酸钠单药治疗癫痫致高同型半胱氨酸血症1例 . 药学实践与服务, 2017, 35(4): 383-384. doi: 10.3969/j.issn.1006-0111.2017.04.024
    [15] 樊鹏程, 葛越, 蒋炜, 景临林, 马慧萍, 贾正平.  线粒体靶向抗氧化剂研究进展 . 药学实践与服务, 2015, 33(1): 1-4,8. doi: 10.3969/j.issn.1006-0111.2015.01.001
    [16] 董雅芬, 舒菁菁, 马靖, 李菲, 彭程, 金磊, 谢和辉, 张川.  天然药物及其活性成分保护内皮祖细胞机制的研究进展 . 药学实践与服务, 2013, 31(1): 11-13,31. doi: 10.3969/j.issn.1006-0111.2013.01.003
    [17] 成彦琼, 张浩, 王威, 顾小飞, 刘爱军.  叶酸在心脑血管疾病防治中的机遇与挑战 . 药学实践与服务, 2013, 31(5): 330-333,350. doi: 10.3969/j.issn.1006-0111.2013.05.003
    [18] 陈迁, 陈孟莉, 叶兆波.  五子衍宗复方总多糖对慢性酒精中毒大鼠肝脏的保护作用 . 药学实践与服务, 2012, 30(1): 25-28,31. doi: 10.3969/j.issn.1006-0111.2012.01.006
    [19] 周恒, 林焕冰, 卓烨烨, 毕炳添, 李国熊, 徐江平.  葡萄籽原花青素对血管性痴呆大鼠空间学习记忆能力的影响 . 药学实践与服务, 2011, 29(3): 208-211.
    [20] 赵宁俭, 赵宁志, 赵仲坤, 张紫洞.  应重视胱氨酸尿症的诊疗 . 药学实践与服务, 1991, (3): 34-35.
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  2931
  • HTML全文浏览量:  310
  • PDF下载量:  373
  • 被引次数: 0
出版历程
  • 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

    全文HTML

参考文献 (24)

目录

    /

    返回文章
    返回

    版权所有：《药学实践与服务》编辑委员会

    主管、主办: 中国人民解放军海军军医大学地址: 上海市杨浦区国和路325号邮政编码: 200433

    电话: （021）81871324,81871397 E-mail: yxsjzzs@163.com

    网站备案号 沪ICP备05003363号-1

    本系统由 北京仁和汇智信息技术有限公司 开发    百度统计