Neuroprotective Effect Of Hyperbaric Oxygen Therapy In Rats With Status Epilepticus

Objective: We investigated the mechanism of neuroprotective effect of hyperbaric oxygen therapy on status epilepticus (SE) in rats. Method: Sixty-three healthy male Sprague-Dawley (SD) rats were randomly divided into two groups: 20 rats in the normal control group, and the remaining 43 rats in SE modeling group by intraperitoneal injection of lithiumhttp://cn.bing.com/dict/search? q=-&FORM=BDVSP6&mkt=zh-cn and pilocarpine. After modeling, the rats were further randomly divided into SE group and hyperbaric therapy group. The onset number of spontaneous epilepsy was recorded by behavioral monitoring. The spatial learning and memory ability of rats were tested by Morris water maze. The neuron number in hippocampus region CA1 was measured by HE staining; YKL-40-positive cells were characterized by immunohistochemistry; nerve cell apoptosis was detected by TUNEL assay; mRNA and protein expressions of Bim and YKL-40 were detected using RT-PCR and Western Blotting, respectively. Results: The onset number of spontaneous seizures was greatly reduced in the hyperbaric oxygen therapy group than in the control group and SE group (P < 0.05). The spatial learning and memory ability of rats in the hyperbaric oxygen therapy group was obviously improved compared with the control group and SE group according to the test using Morris water maze (P < 0.05). Much more neurons were detected in the hippocampus region CA1 in the hyperbaric oxygen therapy group than in the SE group (P < 0.05); immunohistochemistry detection showed that YKL-40-positive cells were greatly reduced in the hyperbaric oxygen therapy group (P < 0.05); according to real-time PCR and Western Blotting detection, the mRNA and protein expressions of Bim and YKL-40 decreased significantly (P < 0.05). Conclusion: Lithiumhttp://cn.bing.com/dict/search?q=-&FORM=BDVSP6&mkt=zh-cn and pilocarpine injection can cause the onset of temporal lobe epilepsy. The hyperbaric oxygen therapy may work by blocking the cell apoptosis pathway mediated by Bim and YKL-40 in rats with SE.