The efficacy role of lycopene inimproving myocardial fibrosis by inhibiting p38 mitogen-activated protein kinases in myocardial infarction rats / 中华老年医学杂志

ABSTRACT

Objective To observe the effect of lycopene on myocardial interstitial fibrosis and to explore the possible mechanisms involved.Methods Sprague-Dawley rat myocardial infarction (MI) model was established by left anterior descending coronary artery ligation.Established MI model rats received lycopene or saline.After 28 days,myocardial fibrosis was observed by Masson staining.The expressions of Ⅰ type collagen,matvix metalloproteina-ses-9 (MMP-9) and matrix metall opeptidaseg(MAPKs) protein were detected in the peri-infarcted zone by Western blotting.Results In MI group,collagen volume fraction (CVF) was increased and the protein expressions of collagen Ⅰ,P-p38 and MMP-9 were increased in the peri-infarcted zone as compared with the sham group [CVF(21.68±4.63)％ vs.(8.21±2.17)％; collagen Ⅰ(1.58±0.22) vs.(0.97±0.09); P-p38(1.93±0.44) vs.(0.85±0.21); MMP-9(4.85±0.47) vs.(1.03±0.59); all P＜0.05].Lycopene attenuated the increments of myocardial infarction-induced collagen Ⅰ,p38MAPK and MMP-9 expressions [collagen Ⅰ(1.24 ± 0.24) vs.(1.58± 0.22) ; P-p38(0.85 ± 0.21) vs.(1.93 ±0.44); MMP9(1.77±0.28) vs.(4.85±0.47); all P＜0.05],and decreased the collagen volume fraction in the peri-infarcted zone [CVF(15.17±2.56)％ vs.(21.68±4.63)％,P＜0.05] as compared with the MI group.Conclusions Lycopene may improve ventricular remodeling after MI by inhibiting p38MAPK signaling pathway and MMP-9 expression.