Introduction: Acute carbon monoxide (CO) poisoning causes serious health problems such as neuropsychological sequelae. This study aimed to investigate neuronal apoptosis and the effects of hyperbaric oxygen (HBO₂) on different regions of the rat hippocampus after CO poisoning.
Methods: 90 mature male Sprague Dawley rats were randomly divided into three groups: the normal control group (NC group), the acute carbon monoxide-poisoned group (CO group) and the hyperbaric oxygen treatment group (HBO₂ group). CO exposure included 0, 1, 3, 7, 14 and 21 treatment days, one exposure on the first day, and sacrifice on each of the following days. HBO₂ exposure included treatment for 0, 1, 3, 7, 14 and 21 days, daily treatment after CO exposure, and sacrifice after the last HBO₂ treatment on each of those days. Hematoxylin-eosin staining, immunohistochemical staining, immunofluorescence staining, and western blot analysis were performed to detect apoptosis in brain tissue samples.
Results: MMP-9 and caspase-3 were prominently increased by CO exposure and inhibited by HBO₂ in the CA3 region in the hippocampus at one, three and seven days (immunohistochemical staining [IHC]: P ⟨ 0.05). Neu N and the ratio of Bcl-2/ BAX were prominently decreased by CO exposure and rescued by HBO₂ in the CA3 region after seven days of treatment (IHC: P ⟨ 0.05).
Conclusion: These findings indicated that neuronal apoptosis in the rat hippocampus could be induced by acute CO exposure, especially in the CA3 region. HBO₂ could effectively inhibit neuronal apoptosis, especially in the CA3 region after seven days of treatment. The application of HBO₂ to inhibit MMP-9 and apoptosis may contribute to brain recovery after acute CO poisoning.
Keywords: carbon monoxide (CO) poisoning; cell apoptosis; hippocampus; hyperbaric oxygen.