Seawater immersion promotes microglia polarization and aggravates neuroinflammatory response
LI Wenxuan
XIE Shengqiang
HE Renke
SU Shichao
XU Ao
WANG Yumeng
YANG Zhijie
WANG Yuxin
LÜ Wenying
CHENG Gang
ZHANG Jianning
Abstract：Objective To explore the impact of seawater immersion on microglial inflammatory polarization and neuroinflammatory responses following traumatic brain injury(TBI),revealing its neuroimmune mechanisms in secondary brain injury.Methods The mouse BV2 microglial cell line was used and divided into blank control group(NC group),seawater immersion group(SW group),LPS-induced group(LPS group),and seawater immersion combined with LPS group(LPS+SW group).The concentration and time of seawater treatment were determined via CCK8 assay.The expression and release of inflammatory cytokine were assessed using qRT-PCR,ELISA,and Western blotting.The level of oxidative stress was evaluated via malondialdehyde(MDA)assay.Results Treatment with 25％artificial seawater for 6 h maintained the viability of BV2 cells within an acceptable range and significantly induced the expression of pro-inflammatory genes such as IL-6,TNF-α,and iNOSS,indicating that seawater has a direct pro-inflammatory effect.On the basis of LPS stimulation,seawater immersion further significantly upregulated IL-6,IL-1β,iNOS,and COX-2 mRNA expression levels,enhanced the release of NO,and suppressed the expression of the anti-inflammatory cytokine IL-10.ELISA results showed that the secretion levels of IL-6 and IL-β in the LPS+SW group were significantly higher than those in the LPS group(P＜0.01).MDA assay showed that LPS could induce significant oxidative stress,while seawater immersion combined with LPS did not further aggravate lipid peroxidation,but the overall state was still oxidative stress.Conclusion Seawater immersion can activate microglia and promote their polarization toward pro-inflammatory phenotypes,and significantly amplify neuroinflammatory responses when combined with LPS,exacerbating neuroimmune dysregulation.This process may form an"inflammation-oxidation"interactive cycle by activating pathways such as NF-κB,and participate in the deterioration of secondary brain injury post-TBI,suggesting the distinct complexity of pathological mechanism of TBI in the marine environment.
Keywords：traumatic brain injurymicrogliaseawater immersionneuroinflammationoxidative stressneuroimmunitycombined injurypolarization
Publication Date：2026-02-28
Online Publishing Date：2026-08-26(First online date of this platform, not the publication date of the document)
Pages：7( 193-199 )