Hyperbaric Oxygen Alleviates the Inflammatory Response Induced by LPS Through Inhibition of NF-κB/MAPKs-CCL2/CXCL1 Signaling Pathway in Cultured Astrocytes.

The purpose of this study was to investigate the inhibition neuroinflammation mechanisms of hyperbaric oxygen therapy (HBOT). Primary astrocytes were incubated with lipopolysaccharide (LPS) after which they underwent HBOT and separate administration of inflammatory cytokine inhibitors. The respective expression of inflammatory factors was then detected. Results showed that LPS significantly induced increases in the expression levels of chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine C-C motif ligand 2 (CCL2), phospho-nuclear factor-kappa B (p-NF-κB), phospho-c-Jun N-terminal kinase (p-JNK), phospho-extracellular signal-regulated kinase (p-ERK), and phospho-p38 (p-p38) in cultured astrocytes and peaked at 3 h. HBOT downregulated the expression of some inflammation mediators including CXCL1 and CCL2. Furthermore, HBOT inhibited the expression of some up-stream regulators of inflammation mediators including p-NF-κB, p-JNK, p-p38 (at 3 and 6 h), and p-ERK (3 h). Inhibitors of NF-κB, ERK, and JNK (BAY117082, PD98059, and SP600125) significantly suppressed the expression of CXCL1 and CCL2 that were induced by LPS for 3 h. However, the p38 inhibitor, SB203580, had no obvious effect on expression levels of CXCL1 and CCL2. In conclusion, we found that HBOT inhibits neuroinflammation via regulation of the LPS-induced NF-κB/mitogen-activated protein kinases (MAPKs, JNK, and ERK) -CCL2/CXCL1 signaling pathways.