Cardioprotective effects of ulinastatin against isoproterenol-induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF-κB pathways.

The purpose of the present study was to evaluate the cardioprotective effect of ulinastatin against isoproterenol‑induced chronic heart failure (CHF). Compared with the control group, treatment with ulinastatin decreased interventricular septal thickness and left ventricular posterior wall thickness, and improved the left ventricular ejection fraction, left ventricular fractional shortening and peak E and peak A ratio in the isoproterenol‑induced CHF rat. In addition, ulinastatin suppressed inflammation, oxidative stress and apoptosis in heart tissue from isoproterenol‑induced CHF rats. Ulinastatin induced the activation of the phosphatidylinositol 3‑kinase (PI3K)/RAC‑α serine/threonine protein kinase (Akt) signaling pathway and downregulated the p38 mitogen‑activated protein kinase (MAPK) and nuclear factor (NF)‑κB pathway in isoproterenol‑induced CHF rats. These data demonstrated the cardioprotective effect of ulinastatin against isoproterenol‑induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF‑κB pathways.