Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury
-
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。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 [Ca2＋]i obviously in Na2S2O4 treated cells in vitro of neonatal rat cardiomyocytes. Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury.
-
Key words:
- 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. -
点击查看大图
计量
- 文章访问数: 2896
- HTML全文浏览量: 326
- PDF下载量: 154
- 被引次数: 0
下载:
