Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

• Autorzy: Gamdzyk M. , Ziembowicz A. , Salinska E.
• Języki publikacji: EN

Abstrakty

PL

Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days old rats, where left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO, HBA (2.5 ATA) and HH (0.5 atm air) were applied at 1, 3 or 6 h after HI for 60 min. Treatment was repeated for 3 following days. Brain injury was assessed by comparing ipsilateral hemisphere and contralateral hemisphere weight. Based on the evaluation of weight ratio, HH, HBO and HBA treatment, regardless of time of treatment initiation, resulted in significant reduction of brain weight loss. We observed that HBO reduced brain damage by 58.1%, 57.6% and 54.9%, respectively to the time of treatment initiation (1, 3, 6 h after HI), HBA decreased the damage by 29.9%, 38.1% and 22.0% (respectively). HH also significantly lessened brain weight loss, from 38% after untreated hypoxia–ischemia to 12.9%, 23.1% and 23.8% after HH application respectively 1, 3 and 6 h after hypoxia–ischemia. Superoxide dismutase (SOD) activity and glutathione (GSH) concentration were also measured. HI caused decrease in GSH concentration and 6-fold increase in SOD activity in ipsilateral, but not contralateral hemisphere. HBO treatment applied 1 and 3 h after HI significantly increased GSH concentration and decreased SOD activity, the effect of HBA was less pronounced. HH treatment resulted in additional increase in SOD activity in both hemispheres. However, GSH concentration after HH returned to control values. HBO and HBA altered the expression of cytoplasmic SOD1, and these changes corresponded to changes in SOD activity, suggesting significant role of this protein in neuroprotecting properties of HBO. Our results suggest that HBO, HBA and HH may serve in attenuation of the effects of HI. Early treatment gives better results in brain protection. Our results suggest that HBO and HBA probably reduce synthesis of free oxygen radicals, which manifests in decreased SOD activity. HH however, seems to act on different mechanism, because it enhances SOD activity. It may be beneficial, as it helps to neutralize superoxide anion production, provided that this SOD activity increase is accompanied by activation of glutathione peroxidase (GPx) and catalase (CAT). This assumption needs further investigation.

Słowa kluczowe

EN

hypobaric hypoxia; hyperbaric treatment; hypoxia; neuronal damage; antioxidative activity; neonatal hypoxia-ischaemia; hypoxic-ischaemic encephalopathy; rat; animal model; brain injury

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2013
• Tom: 73
• Numer: 1
• Opis fizyczny: p.184-185

Twórcy

autor

Gamdzyk M.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Ziembowicz A.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Salinska E.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland