Present situation of ecological benefit of marine oil spill compensation mechanism in China.Oxidative stress and ischemia reperfusion injury are two pivot mechanisms involved in the physiopathology of spinal cord injury.Our recent study found that hyperbaric oxygen preconditioning (HBO-PC) significantly protected the primary cultured rat spinal neurons from oxidative insult and oxygen glucose deprivation via up-regulation of heat shock protein (HSP) 32.In the present study, we further investigated the molecular mechanisms by which HBO-PC induces HSP32 in spinal neurons.Results:HBO-PC significantly activated p38 mitogen-activated protein kinase (p38 MAPK),extracellular regulated protein kinases 1/2 (ERK1/2), and nuclear factor-E2-related factor-2 (Nrf2).The HBO-PC mediated induction of HSP32 and the activation of p38 MAPK and ERK1/2 were significantly inhibited by ROS scavenger (N-Acetyl-L-cysteine, NAC) rather than by NO synthase inhibitor.Pretreatment of cells with SB203580 (p38 MAPK inhibitor) significantly inhibited the expression of HSP32 induced by HBO-PC.Interestingly, ERK1/2 inhibitor (U0126) rather than inhibit the expression of HSP32, but significantly enhanced the induction of HSP32.Innovation and Conclusion: These results suggested that HBO-PC induces HSP32 may through ROS/p38 MAPK/Nrf2 pathway in primary cultured rat spinal neurons and ERK1/2 is a negative regulator in this process.