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

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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

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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.