Hydrogen gas post‑conditioning alleviates cognitive dysfunction and anxiety‑like behavior in a rat model of subarachnoid hemorrhage
- Jing-Hua Song
- Hong-Yan Jia
- Tian-Peng Shao
- Zhi-Bao Liu
- Yuan-Ping Zhao
Affiliations: Department of Radioactive Intervention, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
- Published online on: August 4, 2021 https://doi.org/10.3892/etm.2021.10555
Copyright: © Song
et al. This is an open access article distributed under the
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Subarachnoid hemorrhage (SAH) results in high rates of mortality and lasting disability. Hydrogen gas (H2) is an antioxidant with demonstrated neuroprotective efficacy. The present study examined the therapeutic efficacy of H2 inhalation on early brain injury following experimental SAH in rats and the potential underlying molecular mechanisms. The rats were randomly separated into three groups (n=36 per group): Sham, SAH and SAH + H2. Endovascular perforation of the right internal carotid artery was used to establish SAH. After perforation, rats in the SAH + H2 group inhaled 2.9% H2 with regular oxygen for 2 h. Then, 24 h post‑SAH, TUNEL staining was used to detect apoptotic neurons, and both immunostaining and western blotting were conducted to examine changes in p38 MAPK activity and the expression levels of apoptotic regulators (Bcl‑2, Bax and cleaved caspase‑3) in the ventromedial prefrontal cortex. Then, 30 day post‑SAH, Nissl staining was performed to detect neuronal injury, brain MRI was conducted to detect gross changes in brain structure and metabolism, the open field test was used to assess anxiety and the novel object recognition test was performed to assess memory. H2 inhalation following experimental SAH stabilized brain metabolites, improved recognition memory and reduced anxiety‑like behavior, the neuronal apoptosis rate, phosphorylated p38 MAPK expression, cleaved caspase‑3 expression and the Bax/Bcl‑2 ratio. Collectively, the present results suggested that H2 inhalation can alleviate SAH‑induced cognitive impairment, behavioral abnormalities and neuronal apoptosis in rats, possibly via inhibition of the p38 MAPK signal pathway.