Academic Journal of Second Military Medical University (第二军医大学学报) 2015/36:12 PP.1309-1313
Objective To evaluate the cardioprotective effects of silymarin on mice with acute myocardial infarction (AMI) and its possible mechanism. Methods A total of 60 male C57BL/6 mice were randomly divided into 4 groups: Sham group, AMI group, AMI+Silymarin group, and AMI+Vehicle group. Drug administration was started at the second day after modeling and lasted for four weeks. Four weeks after modeling, hemodynamic parameters and quantitative echocardiographic assessments were obtained to evaluate the cardiac function. Myocardium infarct area was estimated by H-E staining. Cell apoptosis was observed by TUNEL and apoptotic index was calculated. Protein expressions of Bcl-2, Bax and Cleaved Caspase-3 were detected by Western blotting analysis. Results Compared with AMI group, AMI+Silymarin group had improved hemodynamic parameters and cardiac function, significantly reduced infarction area and histopathology changes of the infarcted area (P<0.05), significantly decreased cardiomyocyte apoptotic index (P<0.05), significantly increased protein expression of Bcl-2 and significantly decreased expression of Bax and Cleaved Caspase-3 (P<0.05). Conclusion Silymarin can reduce infarction area and improve cardiac function in mice, which might be related to inhibition of the myocardial apoptosis.
 Hoffmann J, Shmeleva E, Boag S E, Fiser K, Bagnall A, Murali S, et al. Myocardial ischemia and reperfusion leads to transient CD8 immune deficiency and accelerated immunosenescence in CMV-seropositive patients[J].Circ Res, 2015, 116:87-98.
 Vargas-Mendoza N, Madrigal-Santillan E, Morales-Gonzalez A, Esquivel-Soto J, Garcia-Luna Y, Gonzalez-Rubio M, et al. Hepatoprotective effect of silymarin[J]. World Hepatol, 2014, 6: 144-149.
 Rao P R, Viswanath R K. Cardioprotective activity of silymarin in ischemia-reperfusion-induced myocardial infarction in albino rats[J]. Exp Clin Cardiol, 2007, 12: 179-187.
 Zhao J, Agarwal R. Tissue distribution of silibinin, the major active constituent of silymarin, in mice and its association with enhancement of phase Ⅱ enzymes: implications in cancer chemoprevention[J]. Carcinogenesis, 1999, 20: 2101-2108.
 Gao E, Lei Y H, Shang X, Huang Z M, Zuo L, Boucher M, et al. A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse[J].Cric Res, 2010, 107: 1445-1453.
 Xu L, Yates C C, Lockyer P, Xie L, Bevilacqua A, He J, et al. MMI-0100 inhibits cardiac fibrosis in myocardial infarction by direct actions on cardiomyocytes and fibroblasts via MK2 inhibition[J]. J Mol Cell Cardiol, 2014, 77: 86-101.
 Harada M, Qin Y, Takano H, Minamino T, Zou Y, Toko H, et al. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes[J]. Nat Med, 2005, 11: 305-311.
 Kajstura J, Cheng W, Reiss K, Clark W A, Sonnenblick E H, Krajewski S, et al. Apoptotic and necrotic myocyte cell death are independent contributing variables of infarct size in rats[J]. Lab Invest, 1996, 74: 86-107.
 Saraste A, Pulkki K, Kallajoki M, Henriksen K, Parvinen M, Voipio-Pulkki L M. Apoptosis in human acute myocardial infarction[J]. Circulation, 1997, 95: 320-323.
 Yamaguchi M. The anti-apoptotic effect of regucalcin is mediated through multisignaling pathways[J]. Apoptosis, 2013, 18: 1145-1153.
 Biala A K, Kirshenbaum L A. The interplay between cell death signaling pathways in the heart[J]. Trends Cardiovasc Med, 2014, 24: 325-331.