Mechanism of hyperbaric oxygen-regulating inflammatory response through PI3K/AKT pathway after spinal cord injury in rats

Abstract

Objective To explore the effects of hyperbaric oxygen (HBO) on inflammatory response through PI3K/AKT pathway after spinal cord injury (SCI) in rats and investigate the possible mechanism involved. Methods Thirty rats were divided into the HBO group, the HBO combined with PI3K group and the LY294002 group, each consisting of 10 animals. In accordance with the time of spinal cord injury, another 40 rats were divided into 4 groups, i. e. the injury on day 1 group (or the day 1 group), the injury on day 5 group (or the day 5 group), the day 10 group and the control group (the non-injury group), each consisting of 10 animals. One day, 5 and 10 days after spinal cord injury, as well as after HBO therapy, the expression levels of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), p-PI3K, p-AKT and IFN-γ, IL-6 and TNF-α were respectively detected by using Western Blotting and ELISA. The expression levels of IFN-γ, IL-6 and TNF-α in the HBO group, the HBO combined with PI3K group, the LY294002 group and the day one group were detected by using ELISA. Results HBO therapy could significantly increase the expression levels of PI3K, AKT, p-PI3K, p-AKT following spinal cord injury, and decrease the expression levels of IFN-γ, IL-6 and TNF-α(P<0.05). The expression levels of IFN-γ, IL-6 and TNF-α were decreased both in the HBO group and the LY294002 group, however, their expression levels were significantly depressed following over expression of PI3K (P<0.05). Conclusions HBO could significantly inhibit inflammation response after spinal cord injury in rats through the regulation of the PI3K/AKT pathways, indicating that HBO could play an important role in clinical treatment of spinal cord injury, especially in the case of inflammatory response after spinal cord injury. Key words: Hyperbaric oxygen; PI3K/AKT; Rat; Spinal cord injury; Inflammatory response