[1]吴枝娟,余 靖,王瑞幸,等.阿魏酸预处理对阿霉素诱导H9c2心肌细胞损伤的保护作用[J].中国药理学通报,2014,(08):1059.
 WU Zhi-juan,YU Jing,WANG Rui-xing,et al.Protective effect of ferulic acid on doxorubicin induced cellular injury in H9c2 myocardial cells[J].Chinese Pharmacological Bulletin,2014,(08):1059.
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阿魏酸预处理对阿霉素诱导H9c2心肌细胞损伤的保护作用()
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《中国药理学通报》[ISSN:/CN:]

卷:
期数:
2014年08期
页码:
1059
栏目:
论著
出版日期:
2014-08-15

文章信息/Info

Title:
Protective effect of ferulic acid on doxorubicin induced cellular injury in H9c2 myocardial cells
作者:
吴枝娟余 靖王瑞幸方秋娟林默君
福建医科大学基础医学院生理学与病理生理学系,福建 福州 350108
Author(s):
WU Zhi-juan YU Jing WANG Rui-xing FANG Qiu-juan LIN Mo-jun
Dept of Physiology and Pathophysiology, Basic Medical College, Fujian Medical University, Fuzhou 350108, China
关键词:
阿魏酸 阿霉素 心肌保护 H9c2心肌细胞 凋亡 氧化应激
Keywords:
ferulic acid doxorubicin cardioprotection H9c2 myocardial cells apoptosis oxidative stress
分类号:
R-332;R284.1;R322.11;R329.25;R542.202.2;R979.14
文献标志码:
A
摘要:
目的 研究阿魏酸(FA)对阿霉素(DOX)诱导H9c2心肌细胞损伤的影响。方法 1 μmol·L-1 DOX处理H9c2细胞24 h,建立心肌损伤模型。FA预处理组,10、20、40 μmol·L-1 FA预处理2 h后,再与DOX共培养24 h。CCK-8比色法测定细胞生存率; 相差显微镜观察细胞形态学改变; 生化试剂盒检测LDH、CK、MDA、SOD; DCF-DA荧光染色流式细胞术检测细胞内活性氧; AO-EB染色、DNA琼脂糖凝胶电泳检测细胞凋亡; Western blot法测定caspase-3、Bax、Bcl-2表达。 结果 DOX降低H9c2细胞生存率,诱导氧化应激损伤和细胞凋亡。FA预处理剂量依赖性提高细胞生存率,减轻LDH、CK外漏和损伤细胞形态学改变。FA减少ROS生成,降低细胞MDA水平,增加SOD酶活性,抑制DOX诱导的氧化应激。FA下调促凋亡蛋白caspase-3和Bax,上调凋亡抑制蛋白Bcl-2,减少心肌细胞凋亡。 结论 FA可抑制DOX诱导的氧化应激和心肌细胞凋亡,减轻心肌损伤。
Abstract:
Aim To study the effects of ferulic acid(FA)on doxorubicin(DOX)induced cellular injury in H9c2 rat myocardial cells. Methods H9c2 cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit(CCK-8). Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detected by biochemical kits. Intracellular level of reactive oxygen species(ROS)was examined by DCF-DA staining with flow cytometry. Cellular apoptosis was detected by AO-EB staining and DNA agarose gel electrophoresis. The expression of caspase-3, Bax, Bcl-2 was evaluated by Western blot. Results Exposure of H9c2 cells to DOX led to decrease in cell viability, increase in stress and apoptosis. FA pre-treatment improved cell viability in a dose-dependent manner, attenuated leakage of LDH and CK, and reversed morphological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2. Conclusions FA has a protective effect on DOX-induced injury in H9c2 cells. This protection may result from inhibition of myocardial oxidative stress and apoptosis.

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备注/Memo

备注/Memo:
收稿日期:2014-04-08,修回日期:2014-05-12
基金项目:国家自然科学基金资助项目(No 31171104); 福建省自然科学基金资助项目(No 2011J05069); 福建医科大学重点科研基金资助项目(No 09ZD010); 福建医科大学博士启动基金资助项目(No 2010bs007)
作者简介:吴枝娟(1979-),女,博士,讲师,研究方向:心血管药理学,Tel:0591-22862429,E-mail: judywulucy@163.com; 林默君(1964-),男,博士,教授,博士生导师,研究方向:心血管药理学,通讯作者,Tel:0591-22862429,E-mail: mjlin@mail.fjmu.edu.cn
更新日期/Last Update: 1900-01-01