Hyperbaric oxygen ameliorates neuroinflammation in heat-stressed BV-2 microglial cells: potential involvement of...

Heat stroke (HS) is characterized by profound central nervous system (CNS) injury, which drives its high morbidity and mortality. Hyperbaric oxygen therapy (HBO) has been shown to modulate microglial cells in heat-stressed rats, ameliorating neuroinflammation. However, the molecular mechanisms underlying HBO's neuroprotective efficacy remain poorly defined. This study aims to elucidate the neuroprotective effects of HBO on heat-stressed microglial cells and the potential role of microglial EAAT2 in this process.

The control group kept continuously in a 37 °C incubator. The cells in the HS group were exposed to 40 °C for 1 h, followed by 12-h recovery under standard conditions (37 °C, 5% CO₂). The cells in the 0.5 mM DHK+HS group were pretreated with dihydrokainate (DHK) 30 min prior to HS, then processed as above. After the HS+HBO group cells were subjected to HS under the same conditions, hyperbaric oxygen was immediately administered. After the successful modeling of the cells in the 0.5 mM DHK+HS+HBO group, they were pretreated with DHK, exposed to HS, then immediately transferred to HBO before recovery. Cell viability was quantified via CCK-8 assay, while lactate dehydrogenase (LDH) release was assessed colorimetrically. Immunofluorescence, RT-qPCR, and Western blotting were employed to evaluate EAAT2, IL-1β, and IL-10 expression.

Both HBO and DHK can reduce the expression of IL-1β induced by heat stress by inhibiting EAAT2, while upregulating anti-inflammatory IL-10. And the combined treatment has a more significant effect.

HBO alleviates heat stress-induced neuroinflammation by inhibiting microglial EAAT2.