Abstract
Hyperbaric oxygen therapy (HBOT), referring to the medical use of oxygen at a level higher than atmospheric pressure, exerts neuroprotective effects after ischemic stroke via various mechanisms. It has been demonstrated that HBOT modulates the synthesis and degradation of hormones. Leptin, an adipose derived hormone, has been found to confer neuroprotection following experimental stroke. However, it is not known whether HBOT alters leptin concentrations after permanent middle cerebral artery occlusion (pMCAo) in the rat. In this present study, we aimed to investigate the effect of HBOT on the serum concentration of leptin in rats subjected to pMCAo. HBOT was initiated 48 hrs after experimental pMCAo, at 2.5 atmospheres absolutes with 100% oxygen, 1 hr a day for 10 consecutive days. Body weight, neurobehavioral deficits and infarct size were evaluated. Blood was collected on day 1 and day 16 following HBOT. Serum leptin concentrations were measured with ELISA. Delayed HBOT reduced infarct size and improved neurobehavioral scores. Decreased serum levels of leptin were found in treated and untreated pMCAo animals, compared to the sham group on day 1 (P > 0.05) and day 16 (P < 0.05). However, no statistical significance was found between HBOT and the air group. We concluded that the neuroprotective effects of delayed HBOT in pMCAo rats were unlikely to be exerted through changes in the serum concentration of leptin.
Highlights
Hyperbaric oxygen therapy (HBOT) refers to the medical use of oxygen at levels higher than atmospheric pressure
No statistical significance was noted between the air and HBOT groups (P > 0.05)
Serum of treated animals showed no significance compared with that in the serum of air-treated rats (P > 0.05). In this present study, we applied delayed HBOT to permanent middle cerebral artery occlusion (pMCAo) rats in order to explore whether the treatment exerts neuroprotection by modulating the serum concentration of leptin
Summary
Hyperbaric oxygen therapy (HBOT) refers to the medical use of oxygen at levels higher than atmospheric pressure. Recent evidence revealed that HBOT modulates the synthesis and degradation of several hormones Edstrom and his colleagues investigated the effect of HBOT on endocrine organs and found that hyperbaric oxygen evoked adrenal hypertrophy, reduced thymus weight but increased thyroid weight [12]. HBOT (2.0 ATA, 10 days) increased serum levels of estrogen and estrogen receptors in infertile patients [15], and decreased erythropoietin (EPO) concentrations in healthy subjects (2.5 ATA, 90 min) [16]. There is no research related to hormone profiles induced by HBOT in ischemia patients or animal models. It is not clear whether HBOT can ameliorate ischemic brain injury by modulating the serum levels of specific hormones
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