Modified Taohong Siwu Decoction Improved Heart Function After Myocardial Infarction by Inhibiting Inflammatory Factor and Promoting Chemotactic and Pro-Angiogenic Factors

Abstract BackgroundTraditional Chinese medicine has been applied to prevent and treat myocardial infarction (MI) in the clinic for a long history. We recently found that Taohong Siwu decoction (THSWD) exerted a beneficial effect on heart function after MI through improving the local hostile microenvironment. However, the improvement of cardiac function after THSWD administration was moderate. In this study, four Chinese medicine herbs, which have the properties of warming Yang or removing phlegm, were added into THSWD to constitute a new and multifunctional Chinese herbal compound, named modified THSWD (MTHSWD). MethodsA rat model of MI was established by the ligation of left anterior descending coronary artery and MTHSWD was intragastrically administered for 2 weeks. The heart function was examined by echocardiography, cell apoptosis was detected by TUNEL staining and the infarct size was determined by Masson's trichrome staining. The expressions of cytokines, including chemotactic and inflammatory factors, were examined by ELISA in the infarcted myocardium and serum. The level of p-Akt and VEGF in the damaged myocardial tissues was further detected by Western blot. ResultsMTHSWD improved heart function and decreased infarct size and collagen deposition in the infarcted area. In addition, MTHSWD increased the expression of cTnT and Cx43, reduced cell apoptosis in the infarcted area by activating Akt signal and promoted angiogenesis by increasing the expression of VEGF. Interestingly, MTHSWD significantly increased the level of IGF-1, SDF-1 and TNF-α, and significantly reduced the expression of IL-1β in the infarcted myocardium. MTHSWD could also significantly increase the expression of IGF-1, SDF-1 and SCF in the serum. ConclusionsMTHSWD reduced cell apoptosis, promoted angiogenesis and improved heart function after MI probably through the downregulation of inflammatory factor IL-1β, upregulation of chemotactic factors SDF-1 and SCF as well as pro-angiogenic factor VEGF, and activation of Akt signaling pathway.