Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes

Background: Nerol was reported as a natural anti-oxidant product and its protective effects against cardiovascular diseases have been documented. Our current study designed to explore the cardioprotective effect of on hypoxia/reoxygenation (H/R)-induced production reactive oxygen species (ROS) cell apoptosis in H9c2 cells. The potential molecular mechanisms were further investigated.
 Methods: cells treated with 2.5 or 5 µM before after H/R. Lactate dehydrogenase (LDH) release, viability, oxidative stress markers, apoptotic proteins assessed by counting kit-8, LDH release assay, commercial kits, Western blot, respectively. To underlying mechanism, phosphorylation p85 p38, regulatory subunits phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) mitogen-activated protein (MAPK), evaluated blot. confirm that PI3K/AKT signaling pathway participated cardiomyocyte protection, presence absence BEZ235 LY294002 followed H/R treatment.
 Results: remarkably induced apoptosis, ROS production. viability suppressed via inhibiting activation. By contrast, pretreatment can neutralize these activating pathway. With addition LY294002, inhibitory abolished.
 Conclusion: provided promising H/R-induced injuries