Abstract
High-mountain sickness is characterized by brain and pulmonary edema and cognitive deficits. The definition can be fulfilled by a rat model of high-altitude exposure (HAE) used in the present study. This study aimed to investigate the protective effect of hyperbaric oxygen therapy (HBO2T) and to determine the underlying mechanisms. Rats were subjected to an HAE (9.7% O2 at 0.47 absolute atmosphere of 6,000 m for 3 days). Immediately after termination of HAE, rats were treated with HBO2T (100% O2 at 2.0 absolute atmosphere for 1 hour per day for 5 consecutive days) or non-HBO2T (21% O2 at 1.0 absolute atmosphere for 1 hour per day for 5 consecutive days). As compared to non-HAE+non-HBO2T controls, the HAE+non-HBO2T rats exhibited brain edema and resulted in cognitive deficits, reduced food and water consumption, body weight loss, increased cerebral inflammation and oxidative stress, and pulmonary edema. HBO2T increased expression of both hippocampus and lung heat shock protein (HSP-70) and also reversed the HAE-induced brain and pulmonary edema, cognitive deficits, reduced food and water consumption, body weight loss, and brain inflammation and oxidative stress. Decreasing the overexpression of HSP-70 in both hippocampus and lung tissues with HSP-70 antibodies significantly attenuated the beneficial effects exerted by HBO2T in HAE rats. Our data provide in vivo evidence that HBO2T works on a remodeling of brain/lung to exert a protective effect against simulated high-mountain sickness via enhancing HSP-70 expression in HAE rats.
Highlights
High-mountain sickness characterized by cerebral and pulmonary edema and cognitive dysfunction that occurs after high-altitude exposure (HAE) is commonly seen among climbers and tourists [1, 2]
Hyperbaric oxygen (HBO2) preconditioning has been promoted as a promising method for preventing the occurrence of cerebral and pulmonary edema in rats exposed to a simulated HAE [4, 5]
This study provides the following main findings: (i) the HBO2T can increase brain and lung expression of heat shocks protein- (HSP-)70; (ii) the HBO2T can improve passive avoidance learning and spatial memory dysfunction of the rat after HAE; (iii) the HBO2T can attenuate post-HAE cerebral edema; (iv) the HBO2T can reverse post-HAE decreased expression of GSH, decreased expression of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and increased GSSG in the brain; (v) the HBO2T can decrease pot-HAE overexpression of proinflammatory cytokines including IL1β, IL-6, IFN-γ, and tumor necrosis factor-α (TNF-α) in the brain; and (vi) the HBO2T can attenuate post-HAE induction of pulmonary edema and inflammation
Summary
High-mountain sickness characterized by cerebral and pulmonary edema and cognitive dysfunction that occurs after high-altitude exposure (HAE) is commonly seen among climbers and tourists [1, 2]. The high-mountain sickness syndromes displayed by patients can be reproduced by the rats exposed to HAE [3, 4]. Hyperbaric oxygen (HBO2) preconditioning has been promoted as a promising method for preventing the occurrence of cerebral and pulmonary edema in rats exposed to a simulated HAE [4, 5]. Further studies are needed to establish the role of HSP-70 activity in the pathogenesis of high-mountain sickness
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