[Cardioprotective effect and mechanism of post-infarction ventricular remodeling after self-assembling peptide and thermosensitive hydrogel implantation in rat myocardial infarction model]

Abstract

Objective: To compare the cardioprotective effect of self-assembling peptide (RAD16-II) and thermosensitive hydrogel DPHP (Dex-PCL-HEMA/PNIPAAm) and investigate the optimal property of hydrogel for the treatment of myocardial infarction (MI).

Methods: MI model was induced by left anterior descending (LAD) coronary artery ligation in SD rats. The animals were randomized into three groups to receive RAD16-II hydrogel (n = 15), DPHP hydrogel (n = 15) or PBS (phosphate buffered saline; control group n = 15); sham-operated rats (n = 10), a suture was tied loosely around left coronary artery without ligating it. At Day 20 post-MI, left ventricle function was evaluated by echocardiography and cardiac catheter. Masson's trichrome was used for histological examination; anti-alpha-smooth muscle antigen (alpha-SMA) was applied to label the neovasculature formation in infarct area.

Results: The rats receiving DPHP hydrogel showed a significantly smaller left ventricle end diastolic diameter (LVEDd) and higher levels of left ventricle fraction shortening (LVFS) and left ventricle end systolic pressure (LVESP) than the rats in RAD16-II group [LVEDd (7.9 +/- 0.9) mm vs (8.9 +/- 0.8) mm]; [LVFS (25.4 +/- 5.1)% vs (21.9 +/- 2.9)%; LVESP (114.0 +/- 7.6) mm Hg vs (99.1 +/- 9.6) mm Hg; P < 0.05]. Histological examination showed uncompleted degraded hydrogel in infarct area of DPHP group but not in RAD16-II group. The animals receiving DPHP hydrogel demonstrated significantly a smaller infarct size, a higher infarct wall thickness and a lower vessel density in infarct than the animals receiving RAD16-II hydrogel (P < 0.05).

Conclusion: DPHP hydrogel implantation further inhibits the post-MI ventricle remodeling than RAD16-II hydrogel implantation. The mechanism is not correlated with the vascular density in infarct area.