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Turk J Med Sci. 2016 Nov 17;46(5):1534-1539. doi: 10.3906/sag-1502-3.

The protective effects of hydrogen on HO-1 expression in the brainafter focal cerebral ischemia reperfusion in rats.

Author information

1
Department of Critical Care Medicine, Yu Huang Ding Hospital, Qingdao University, Yan Tai, P.R. China.
2
Department of Histology and Embryology, Bin Zhou Medical College, Yan Tai, P.R. China.

Abstract

BACKGROUND/AIM:

The aim of this study was to investigate whether a hydrogen administration can produce neuroprotective effects after brain ischemia reperfusion in rats.

MATERIALS AND METHODS:

A brain ischemia reperfusion injury was induced by a 2-h left middle cerebral artery occlusion (MCAO) using an intraluminal filament, followed by 46 h of reperfusion. A hydrogen-rich saline (1 mL/kg body weight i.p.) was administered at the beginning of reperfusion. Saline (1 mL/kg)-treated animals were used as the control. Sham-operated animals were also used. Subsequently, 48 h after the MCAO, histological alternations, heme oxygenase-1 (HO-1) expression, and levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the cerebral cortex and the hippocampus were examined.

RESULTS:

Hydrogen significantly alleviated brain tissue histological damage, promoted HO-1 expression, upregulated levels of SOD, and decreased the levels of MDA in brain tissue after the ischemia reperfusion injury.

CONCLUSION:

The results suggest that the neuroprotective effects of hydrogen may be mediated by promoting HO-1 expression and attenuated the oxidative injury.

KEYWORDS:

Hydrogen; brain; cerebral ischemia reperfusion; heme oxygenase-1; rats

PMID:
27966325
DOI:
10.3906/sag-1502-3
[Indexed for MEDLINE]

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