Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Jinan, Shandong 250012, China ; Department of Traditional Chinese Medicine, Qilu Hospital, Shandong University, No. 107, Wen Hua Xi Road, Jinan, Shandong 250012, China.
Evid Based Complement Alternat Med. 2013;2013:813247. doi: 10.1155/2013/813247. Epub 2013 Aug 27.
Background. Myocardial infarction (MI) is a major cause of morbidity and mortality in the world. Tongxinluo (TXL) is a traditional Chinese compound prescription which has cardioprotective functions. The present study was aimed to determine the effect of TXL on postischemic cardiac dysfunction and cardiac remodeling and to elucidate the underlying mechanisms. Methods and Results. MI was performed by ligation of left anterior descending coronary artery (LAD) in male adult mice. Mice were randomly divided into four groups: (1) sham group (Sham); (2) MI-control group (Control); (3) MI-low dose TXL group (TXL-L); and (4) MI-high dose TXL (TXL-H) group. Compared with the control group, TXL treatment restored cardiac function, increased revascularization, attenuated cardiomyocyte apoptosis, and reduced interstitial fibrosis. TXL treatment increased the phosphorylation of Akt, extracellular signal regulated kinase (ERK), and endothelial nitric oxide synthase (eNOS); the expression of phosphatidylinositol3-kinase (PI3K), hypoxia-inducible factors 1 α (HIF-1 α ), and vascular endothelial growth factor (VEGF); and the DNA binding activity of HIF-1 α after MI. Conclusion. TXL may improve cardiac function and ameliorate cardiac remodeling by increasing neovascularization through enhancing the phosphorylation of Akt and ERK, the expression and activity of HIF-1 α , and the protein level of VEGF and p-eNOS.
心肌梗死(MI)是世界范围内发病率和死亡率的主要原因。通心络(TXL)是一种具有心脏保护功能的中药复方。本研究旨在确定 TXL 对缺血后心功能障碍和心脏重构的影响,并阐明其潜在机制。
通过结扎雄性成年小鼠的左前降支冠状动脉(LAD)来进行 MI。将小鼠随机分为四组:(1)假手术组(Sham);(2)MI-对照组(Control);(3)MI-低剂量 TXL 组(TXL-L);和(4)MI-高剂量 TXL 组(TXL-H)。与对照组相比,TXL 治疗恢复了心脏功能,增加了再血管化,减弱了心肌细胞凋亡,并减少了间质纤维化。TXL 治疗增加了 Akt、细胞外信号调节激酶(ERK)和内皮型一氧化氮合酶(eNOS)的磷酸化;磷脂酰肌醇 3-激酶(PI3K)、缺氧诱导因子 1α(HIF-1α)和血管内皮生长因子(VEGF)的表达;以及 HIF-1α 在 MI 后的 DNA 结合活性。
TXL 可能通过增强 Akt 和 ERK 的磷酸化、HIF-1α 的表达和活性以及 p-eNOS 的蛋白水平,增加新生血管形成,从而改善心功能和心脏重构。