Inhaled molecular hydrogen attenuates intense acute exercise-induced hippocampal inflammation in sedentary rats.

Abstract

This study examined whether inhaled molecular hydrogen (2% H2) modulates hippocampal inflammation and oxidative stress in sedentary rats subjected to intense acute treadmill exercise. Animals ran in a sealed chamber while breathing either 2% H2 or a control gas mixture. Hippocampal tissue was collected immediately and 3 hours post-exercise. Exercise elevated TNF-α, IL-6, and IL-10 immediately after the session, with no change in IL-1β. H2 inhalation suppressed the exercise-induced rises in TNF-α and IL-6 while further amplifying the IL-10 response. Oxidative stress markers—SOD activity, TBARS, and NOx—were unaffected by either exercise or H2. All measured parameters returned to baseline levels by 3 hours post-exercise. These findings indicate that H2 exerts anti-inflammatory effects in the hippocampus by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokine production, without altering local oxidative stress status.

Mechanism

H2 inhalation reduces exercise-induced hippocampal inflammation by suppressing pro-inflammatory cytokines TNF-α and IL-6 while simultaneously enhancing the anti-inflammatory cytokine IL-10, without altering oxidative stress markers such as SOD, TBARS, or NOx.