Hydrogen-rich water protects against ischemic brain injury in rats by regulating calcium buffering proteins.

Abstract

This study examined whether hydrogen-rich water (HRW) could influence the expression of two calcium-buffering proteins, parvalbumin and hippocalcin, in the context of cerebral ischemia and glutamate-induced neuronal death. Male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO), and HRW (6 ml/kg) was administered before and after the procedure. Cortical tissue was collected at 1, 7, and 14 days post-MCAO. HRW-treated animals showed reduced infarct volume and improved neurological scores. Ischemia-induced decreases in parvalbumin and hippocalcin levels were prevented by HRW in vivo. In vitro experiments demonstrated that HRW dose-dependently reduced glutamate toxicity-associated neuronal death and suppressed the accompanying rise in intracellular Ca²⁺ concentration. These findings indicate that preservation of calcium-buffering protein levels may contribute to the neuroprotective mechanism of HRW during ischemic brain injury.

Mechanism

HRW preserves the expression of calcium-buffering proteins parvalbumin and hippocalcin, thereby attenuating intracellular Ca²⁺ overload triggered by glutamate toxicity and ischemia-reperfusion, which reduces neuronal apoptosis.