Propofol postconditioning protects H9c2 cells from hypoxia/reoxygenation injury by inducing autophagy via the SAPK/JNK pathway.

Propofol postconditioning (P‑PostC) offers cardioprotection in mice, and the upregulation of autophagy protects cardiac cells against ischemia/reperfusion injury. The present study aimed to examine the effects of P‑PostC on the induction of autophagy and its potential roles in hypoxia/reoxygenation (H/R) injury. Rat heart‑derived H9c2 cells were exposed to H/R, comprising 6 h of hypoxia followed by 4 h of reoxygenation, as well as postconditioning with various concentrations of propofol at the onset of reperfusion. Lactate dehydrogenase (LDH) activity and the rate of cell apoptosis were measured to evaluate the degree of cardiomyocyte H/R injury. The induction of autophagy in myocytes subjected to H/R injury and P‑PostC was detected by western blotting and immunofluorescence. Furthermore, the activation of c‑Jun N‑terminal kinase (JNK) in cells treated with P‑PostC with or without co‑treatment with SP600125, an inhibitor of JNK, was also determined by western blotting. P‑PostC reduced the activity of LDH in the culture medium and the percentage of apoptotic cells compared with cells in the untreated H/R group. In addition, P‑PostC induced autophagy and promoted survival signaling in H9c2 cardiac myoblast cells. The inhibition of autophagy by 3‑methyladenine treatment diminished the cardioprotective effects of P‑PostC. These results indicated that propofol postconditioning promoted cell survival through the induction of autophagy in H9c2 cardiac cells, and that the stress‑activated protein kinase/JNK survival pathway may be partly involved in P‑PostC‑induced autophagy.