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

  • Jin Cheng Department of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, China
  • Qing Zou Department of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, China
  • Yugang Xue Department of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, China
Keywords: Nerol, Oxidative stress, Hypoxia/reoxygenation, Apoptosis, PI3K/AKT signaling


Background: Nerol was reported as a natural anti-oxidant product and its protective effects against cardiovascular diseases have been documented. Our current study was designed to explore the cardioprotective effect of Nerol on hypoxia/reoxygenation (H/R)-induced production of reactive oxygen species (ROS) and cell apoptosis in H9c2 cells. The potential molecular mechanisms were further investigated.

Methods: The cells were treated with 2.5 or 5 µM Nerol before or after H/R. Lactate dehydrogenase (LDH) release, cell viability, oxidative stress markers, and apoptotic proteins were assessed by cell counting kit-8, LDH release assay, commercial kits, and Western blot, respectively. To explore the underlying mechanism, the phosphorylation of p85 and p38, regulatory subunits of phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase (MAPK), was evaluated by Western blot. To further confirm that the PI3K/AKT signaling pathway participated in the cardiomyocyte protection, H9c2 cells were treated with 5 µM Nerol in the presence or absence of 5 µM BEZ235 or LY294002 followed by H/R treatment.

Results: H/R remarkably induced apoptosis, LDH release and ROS production. The cell viability was suppressed via inhibiting the PI3K/AKT signaling pathway activation. By contrast, pretreatment with Nerol can neutralize these effects by activating the PI3K/AKT signaling pathway. With the addition of BEZ235 or LY294002, the inhibitory effects of Nerol were abolished.

Conclusion: Nerol provided promising cardioprotective effect against H/R-induced injuries in H9c2 cells by activating the PI3K/AKT pathway.


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How to Cite
ChengJ., ZouQ., & XueY. (2021). Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes. STEMedicine, 2(6), e87.
Research articles