新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究

程晶晶; 刘谋治; 李洪娇; 阎澜; 姜远英; 颜天华

doi:10.3969/j.issn.1006-0111.2014.06.010

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！

新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究

程晶晶, 刘谋治, 李洪娇, 阎澜, 姜远英, 颜天华

文章导航 > 药学实践与服务 > 2014 > 32(6): 440-443

程晶晶, 刘谋治, 李洪娇, 阎澜, 姜远英, 颜天华. 新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究[J]. 药学实践与服务, 2014, 32(6): 440-443. doi: 10.3969/j.issn.1006-0111.2014.06.010

引用本文:

CHENG Jingjing, LIU Mouzhi, LI Hongjiao, YAN Lan, JIANG Yuanying, YAN Tianhua. Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 440-443. doi: 10.3969/j.issn.1006-0111.2014.06.010

Citation:

CHENG Jingjing, LIU Mouzhi, LI Hongjiao, YAN Lan, JIANG Yuanying, YAN Tianhua. Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 440-443. doi: 10.3969/j.issn.1006-0111.2014.06.010

新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究

doi: 10.3969/j.issn.1006-0111.2014.06.010

1.
武警河南省总队医院药剂科, 河南郑州 450000
2.
中国药科大学药学院, 江苏南京 210009
3.
第二军医大学附属长海医院, 上海 200433
4.
第二军医大学药学院, 上海 200433

Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury

1.
Department of Pharmacy, Henan People's Armed Police Corps Hospital, Zhengzhou 450000, China
2.
School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China
3.
Changhai Hospital Affiliated to Second Military Medical University, Shanghai 200433, China
4.
School of Pharmacy, Second Military Medical University, Shanghai 200433, China

摘要: 目的研究TG6对心肌缺血/再灌注损伤的保护作用及机制。方法采用整体大鼠心肌缺血/再灌注(I/R)实验,离体大鼠心脏低灌复灌实验和乳鼠心肌细胞缺氧/复氧损伤(H/R)实验等模型,以血清CK、LDH、T-SOD、MDA等为指标,研究TG6对心肌缺血再灌注损伤的保护作用。结果在整体大鼠心肌缺血再灌注损伤实验中,TG6显著减少I/R损伤后心肌梗死面积,减少血清中CK活力和MDA含量,减少LDH活力,增加T-SOD活力;在离体大鼠心脏低灌复灌实验中,TG6显著增加低灌复灌后心肌冠脉流量,减少心肌组织中MDA含量和CK、LDH外漏,提高心肌组织中T-SOD活力;在乳鼠心肌细胞H/R损伤实验中,TG6对正常生长条件下的细胞没有明显影响,提高Na₂S₂O₄制备的心肌细胞H/R模型下细胞的存活率、降低细胞CK的释放率及细胞[Ca²⁺]_i的含量。结论 TG6对心肌I/R损伤有一定的保护作用。
- 钠氢交换器抑制剂 /
- 心肌缺血/再灌注 /
- 冠脉结扎 /
- 离体心脏灌流 /
- 心肌细胞 /
- 缺氧/复氧
Abstract: Objective To investigate the protective effects and mechanism of TG6 on myocardial ischemia/reperfusion injury. Methods the protective effects of TG6 on myocardial ischemia/reperfusion was investigated by setting up models of ischemia and reperfusion of rats induced by ligating the left coronary anterior descending artery in vivo,isolated rat hearts through an improved Langendorff device, and hypoxia /reoxygenation injury of neonatal rat cardiomyocytes, and the serum CK,LDH,T-SOD, MDA were taken as research markers. Results TG6 significantly reduced the myocardial infarct size, decreased the activity of CK and the content of MDA in serum, reduced the activity of LDH, and increased the activity of T-SOD in vivo;TG6 obviously increased the coronary blood flow after low rate perfusion and reperfusion, decreased the content of MDA and the leakage of CK, LDH in myocardial tissue, elevated the activity of T-SOD in vitro of isolated rat hearts;TG6 had no effects on cells in normal growth condition, raised the viability of cardiomyocytes significantly, and reduced the rate of CK leakage and the content of [Ca^2＋]_i obviously in Na₂S₂O₄ treated cells in vitro of neonatal rat cardiomyocytes. Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury.
- NHEI /
- myocardial ischemia/reperfusion /
- coronary artery ligation /
- isolated heart perfusion /
- cardiomyocyte /
- H/R

[1]	石燕燕, 李树青. 心肌缺血再灌注损伤治疗进展[J].中国心血管病研究, 2007, 5(10):777-779.
[2]	胡若愚. 钠氢通道抑制剂在心脏缺血再灌注损伤中的保护作用[J].实用医学杂志, 2006, 22(24):2931-2933.
[3]	Lee SH, Kim T, Park ES, et al. NHE10, a novel osteoclast-specific member of the Na⁺-H⁺ exchanger family, regulates osteoclast differentiation and survival[J].Biochem Biophys Res Commun, 2008, 369(2):320-326.
[4]	Kim JC, Woo SH. Role of Na⁺-H⁺ exchange in the modulation of L-type Ca²⁺ current during fluid pressure in rat ventricular myocytes[J].Biochem Biophys Res Commun,2013,431(2): 239-245.
[5]	徐叔云, 卞如濂, 陈修. 药理实验方法学[M].3版.北京:人民卫生出版社, 2002:1042-1052.
[6]	戴小燕,方秋娟. Langendorff离体心脏灌注模型的制备及应用[J].医学综述,2012,(13):2036-2039.
[7]	司徒镇强,吴军正.细胞培养[M].2版, 世界图书出版公司,2008:200-201.
[8]	许蜀闽,王培勇,马红英,等. 连二亚硫酸钠在建立培养细胞的无氧环境中的应用[J].第三军医大学学报, 2005, 27(4):359-360.
[9]	张新宁,吕琪, 张永亮,等. 大鼠心肌缺血再灌注模型建立方法的改进[J]. 武警医学院学报, 2008,17(11):941-943.
[10]	周燕. 心肌损伤标志物的研究进展与心肌梗死的诊断标准[J]. 临床医学,2009,22(12):2860-2862.
[11]	Zhu X, Zuo L. Characterization of oxygen radical formation mechanism at early cardiac ischemia[J].Cell Death Dis,2013,4:e787.
[12]	赵芳, 徐立, 许立. 参附注射液对大鼠离体心脏缺血再灌注损伤的作用[J].中药新药与临床药理, 2007, 18(1):17-19.
[13]	王丽艳, 刘艳, 李丹露,等. 胆碱对离体大鼠心肌缺血/再灌注损伤的保护作用[J].中国药理学通报, 2007, 23 (5):600-603.
[14]	许蜀闽, 王培勇, 马红英,等. 连二亚硫酸钠在建立培养细胞的无氧环境中的应用[J].第三军医大学学报, 2005, 27(4):359-360.
[15]	Shintani-Ishida K, Inui M, Yoshida K. Ischemia-reperfusion induces myocardial infarction through mitochondrial Ca²⁺ overload[J]. J Mol Cell Cardiol,2012,(53):233-239.

[1]	张艺昕, 关欣怡, 王博宁, 闻俊, 洪战英. 二氢吡啶类钙离子拮抗药物手性分析及其立体选择性药动学研究进展 . 药学实践与服务, 2024, 42(8): 319-324. doi: 10.12206/j.issn.2097-2024.202308062
[2]	夏哲炜, 曾垣烨, 朱海菲, 李育, 陈啸飞. 核磁共振磷谱法测定磷酸氢钙咀嚼片中药物含量 . 药学实践与服务, 2024, 42(9): 399-401, 406. doi: 10.12206/j.issn.2097-2024.202404063
[3]	陈春娟, 郑志新, 李骊. 平喘方联合孟鲁司特钠治疗儿童支气管哮喘患者的临床疗效观察 . 药学实践与服务, 2024, 42(): 1-5. doi: 10.12206/j.issn.2097-2024.202405035
[4]	崔亚玲, 吴琼, 马良煜, 胡北, 姚东, 许子华. 肝素钠肌醇烟酸酯乳膏中肌醇烟酸酯皮肤药动学研究 . 药学实践与服务, 2024, 42(): 1-5. doi: 10.12206/j.issn.2097-2024.202404006
[5]	刘丽艳, 余小翠, 孙传铎. 纳武利尤单抗治疗非小细胞肺癌有效性及安全性的Meta分析 . 药学实践与服务, 2024, 42(10): 451-456. doi: 10.12206/j.issn.2097-2024.202310044
[6]	迟文雅, 袁艳, 李伟林, 吴茼妤, 俞媛. 负载骨髓间充质干细胞/白藜芦醇脂质体的水凝胶支架用于创伤性脑损伤治疗 . 药学实践与服务, 2024, 42(): 1-8. doi: 10.12206/j.issn.2097-2024.202406034
[7]	宋雨桐, 夏德润, 顾珩, 唐少文, 易洪刚, 沃红梅. 帕博利珠单抗与铂类化疗方案在晚期非小细胞肺癌一线治疗中的药物经济学评价 . 药学实践与服务, 2024, 42(8): 334-340. doi: 10.12206/j.issn.2097-2024.202303023
[8]	冯志惠, 邓仪卿, 叶冰, 安培, 张宏, 张海军. 雀梅藤石油醚提取物诱导三阴性乳腺癌细胞凋亡的实验研究 . 药学实践与服务, 2024, 42(6): 253-259. doi: 10.12206/j.issn.2097-2024.202311055
[9]	修建平, 杨朝爱, 刘禧澳, 潘乾禹, 韦广旭, 王卫星. 全反式维甲酸对肝星状细胞活化及氧化应激的作用和机制探索 . 药学实践与服务, 2024, 42(7): 291-296. doi: 10.12206/j.issn.2097-2024.202312054
[10]	姜涛, 徐卫凡, 蒋益萍, 夏天爽, 辛海量. 巴戟天丸组方对Aβ损伤成骨细胞的作用及基于网络药理学的机制研究 . 药学实践与服务, 2024, 42(7): 285-290, 296. doi: 10.12206/j.issn.2097-2024.202305011
[11]	王晓飞, 张颖, 顾佳钰, 胡馨儿, 张海, 曹岩. 表面等离子共振传感器的识别元件在医药领域中的研究应用进展 . 药学实践与服务, 2024, 42(): 1-9. doi: 10.12206/j.issn.2097-2024.202309014
[12]	毛智毅, 王筱燕, 陈晓颖, 汤逸斐. 度拉糖肽联合二甲双胍对肥胖型2型糖尿病患者机体代谢、体脂成分及血清脂肪因子的影响 . 药学实践与服务, 2024, 42(7): 305-309. doi: 10.12206/j.issn.2097-2024.202305032
[13]	张广雨, 杜晶, 刘梦珍, 朱丹妮, 闫慧, 刘冲. 新斯的明与山莨菪碱联合应用对肺型氧中毒的保护作用及其机制的研究 . 药学实践与服务, 2024, 42(10): 433-438, 444. doi: 10.12206/j.issn.2097-2024.202310049
[14]	杨媛媛, 安晓强, 许佳捷, 江键, 梁媛媛. 正极性驻极体联合5-氟尿嘧啶对瘢痕成纤维细胞生长抑制的协同作用 . 药学实践与服务, 2024, 42(6): 244-247. doi: 10.12206/j.issn.2097-2024.202310027
[15]	刘汝雄, 杨万镇, 涂杰, 盛春泉. 铁死亡调控蛋白GPX4的小分子抑制剂研究进展 . 药学实践与服务, 2024, 42(9): 375-378. doi: 10.12206/j.issn.2097-2024.202312075

点击查看大图

计量

文章访问数: 2828
HTML全文浏览量: 319
PDF下载量: 154
被引次数: 0

新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究

doi: 10.3969/j.issn.1006-0111.2014.06.010

1. 武警河南省总队医院药剂科, 河南郑州 450000

2. 中国药科大学药学院, 江苏南京 210009

3. 第二军医大学附属长海医院, 上海 200433

4. 第二军医大学药学院, 上海 200433

收稿日期: 2013-10-09
修回日期: 2014-03-19

关键词:

摘要: 目的研究TG6对心肌缺血/再灌注损伤的保护作用及机制。方法采用整体大鼠心肌缺血/再灌注(I/R)实验,离体大鼠心脏低灌复灌实验和乳鼠心肌细胞缺氧/复氧损伤(H/R)实验等模型,以血清CK、LDH、T-SOD、MDA等为指标,研究TG6对心肌缺血再灌注损伤的保护作用。结果在整体大鼠心肌缺血再灌注损伤实验中,TG6显著减少I/R损伤后心肌梗死面积,减少血清中CK活力和MDA含量,减少LDH活力,增加T-SOD活力;在离体大鼠心脏低灌复灌实验中,TG6显著增加低灌复灌后心肌冠脉流量,减少心肌组织中MDA含量和CK、LDH外漏,提高心肌组织中T-SOD活力;在乳鼠心肌细胞H/R损伤实验中,TG6对正常生长条件下的细胞没有明显影响,提高Na₂S₂O₄制备的心肌细胞H/R模型下细胞的存活率、降低细胞CK的释放率及细胞[Ca²⁺]_i的含量。结论 TG6对心肌I/R损伤有一定的保护作用。

English Abstract

Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury

1. Department of Pharmacy, Henan People's Armed Police Corps Hospital, Zhengzhou 450000, China

2. School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China

3. Changhai Hospital Affiliated to Second Military Medical University, Shanghai 200433, China

4. School of Pharmacy, Second Military Medical University, Shanghai 200433, China

Received Date: 2013-10-09
Rev Recd Date: 2014-03-19

Keywords:

Abstract: Objective To investigate the protective effects and mechanism of TG6 on myocardial ischemia/reperfusion injury. Methods the protective effects of TG6 on myocardial ischemia/reperfusion was investigated by setting up models of ischemia and reperfusion of rats induced by ligating the left coronary anterior descending artery in vivo,isolated rat hearts through an improved Langendorff device, and hypoxia /reoxygenation injury of neonatal rat cardiomyocytes, and the serum CK,LDH,T-SOD, MDA were taken as research markers. Results TG6 significantly reduced the myocardial infarct size, decreased the activity of CK and the content of MDA in serum, reduced the activity of LDH, and increased the activity of T-SOD in vivo;TG6 obviously increased the coronary blood flow after low rate perfusion and reperfusion, decreased the content of MDA and the leakage of CK, LDH in myocardial tissue, elevated the activity of T-SOD in vitro of isolated rat hearts;TG6 had no effects on cells in normal growth condition, raised the viability of cardiomyocytes significantly, and reduced the rate of CK leakage and the content of [Ca^2＋]_i obviously in Na₂S₂O₄ treated cells in vitro of neonatal rat cardiomyocytes. Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury.