Inhaled molecular hydrogen reduces hippocampal neuroinflammation, glial reactivity and ameliorates memory impairment during systemic inflammation.

Abstract

Using a rat endotoxemia model induced by a single lipopolysaccharide (LPS) injection, this study examined how inhaled molecular hydrogen (H2) affects hippocampal neuroinflammation during systemic inflammation. Integrating approaches from hippocampal electrophysiology to behavioral testing, the investigators found that H2 inhalation reduced pro-inflammatory cytokine levels in both peripheral blood and hippocampal tissue. Microglial and astrocytic activation were also diminished. Behavioral assessments revealed attenuation of memory impairment, whereas long-term potentiation (LTP) remained unaffected. These findings represent the first reported evidence that inhaled H2 can suppress hippocampal microglial and astrocytic inflammatory responses, an effect associated with reduced cognitive deficits arising from systemic inflammation.

Mechanism

Inhaled H2 appears to reduce LPS-induced pro-inflammatory cytokine surges in the hippocampus by suppressing microglial and astrocytic activation, thereby limiting neuroinflammation and associated memory deficits without altering long-term potentiation.