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中国应用生理学杂志 ›› 2017, Vol. 33 ›› Issue (2): 159-163.doi: 10.12047/j.cjap.5446.2017.040

• 研究论文 • 上一篇    下一篇

碱性成纤维生长因子对大鼠成肌细胞氧化应激损伤的作用及其机制

毛挺挺1, 方红波1, 王晓慧2, 潘莹莹2, 谢浩煌2, 张宏宇2, 肖健2, 姜丽萍3   

  1. 1. 宁波市医疗中心李惠利东部医院, 浙江 宁波 315000;
    2. 温州医科大学, 浙江 温州 325035;
    3. 上海交通大学附属新华医院, 上海 200092
  • 收稿日期:2016-04-11 修回日期:2016-11-22 出版日期:2017-03-28 发布日期:2018-06-20
  • 通讯作者: 姜丽萍,Tel:13868311990,E-mail:ljpingj@shsmu.edu.cn E-mail:ljpingj@shsmu.edu.cn
  • 基金资助:
    国家自然科学基金(81372064);上海市教委护理高原学科建设资助项目

Effects and mechanism of bFGF on rat myoblast oxidative injury induced by hydrogen peroxide

MAO Ting-ting1, FANG Hong-bo1, WANG Xiao-hui2, PAN Ying-ying2, XIE Hao-huang2, ZHANG Hong-yu2, XIAO Jian2, JIANG Li-ping3   

  1. 1. Ningbo Medical Center Lihuili Eastern Hospital, Ningbo 315000;
    2. Wenzhou Medical University, Wenzhou 325035;
    3. Xinhua Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200092, China
  • Received:2016-04-11 Revised:2016-11-22 Online:2017-03-28 Published:2018-06-20
  • Supported by:
    国家自然科学基金(81372064);上海市教委护理高原学科建设资助项目

摘要: 目的:探讨碱性成纤维生长因子(bFGF)下调氧自由基水平在大鼠成肌细胞氧化应激中的保护作用。方法:采用对数生长期大鼠成肌细胞,随机分为四组(n=6):正常对照组(control),单纯bFGF组(bFGF),氧化应激组(H2O2),干预组(bFGF+H2O2)。氧化应激组采用含100μmol/L H2O2的培养基继续孵育4 h。免疫组化检测B淋巴细胞瘤-2基因(Bcl-2)阳性沉积颗粒;免疫荧光观察活性氧自由基(ROS)水平、Bcl-2、B淋巴细胞瘤-2基因相关X蛋白(Bax)及细胞色素C(Cyt.C)表达;Western blot检测Cyt.C、聚腺苷二磷酸核糖聚合酶(PARP)蛋白表达情况。结果:与正常组比较,氧化应激组成肌细胞Bcl-2表达降低,ROS、Cyt.C表达显著增加(P < 0.05)。与氧化应激组比较,bFGF干预后的成肌细胞Bcl-2表达增加,ROS及Cyt.C表达减少(P < 0.05)。结论:bFGF对成肌细胞氧化应激具有保护作用,其机制可能与bFGF下调氧自由基水平、Bcl-2蛋白增加、Cyt.C表达减少有关。

关键词: 压疮深部组织损伤, 氧化应激, 大鼠成肌细胞, bFGF

Abstract: Objective: To explore the protective role of basic fibroblast growth factor (bFGF) on attenuating hydrogen peroxide-induced injury in cultured rat myoblasts. Methods: Cultured rat myoblasts at growth phase were randomly divided into four groups (n=6):control group (control), bFGF group (bFGF), model group(H2O2) and the treatment group (bFGF + H2O2). Model group was treated with 100 μmol/L hydrogen peroxide for 4h. B-cell lymphoma-2 (Bcl-2) positive particles were detected by immunohistochemistry; Reactive oxygen species (ROS) and expression for Bcl-2 associated X protein (Bax), Bcl-2 and Cytochrome C (Cyt. C) fluorescence were observed under the invented microscope; Cyt. C and Poly ADP-ribose polymerase(PARP)protein were assessed by Western blot. Results: Compared with control group, the myoblats in the model group showed low expression of Bcl-2 positive particles, accompanied by high expression of ROS level and Cyt. C fuorescence (P < 0.05); Compared with model group, bFGF enhanced Bcl-2 activity of the myoblasts, and significantly downregulated Cyt. C and PARP expression (P < 0.05). Conclusion: bFGF could attenuate oxidative injury of rat myoblasts induced by hydrogen peroxide, which mechanism might be related to enhanced Bcl-2 and reduced ROS, Cyt. C levels.

Key words: pressure ucler, deep tissue injury, oxidative stress, rat myoblasts

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