摘要
目的观察早期高压氧(hyperbaric oxygen,HBO)暴露对实验大鼠脑外伤后水通道蛋白-4 (aquaporin-4,AQP-4)和半胱天冬酶-3(caspase-3)的影响,探讨高压氧对脑外伤的治疗作用及脑保护的分子生物机制。方法采用Feeney自由落体法建立大鼠脑外伤模型,将大鼠随机分为假手术组、创伤组和HBO组,HBO组在损伤后1 h内给予高压氧治疗,第4天用干湿重法测脑组织含水量、免疫组织化学法及图像分析技术检测AQP-4和caspase-3,用双重染色免疫组化法检测AQP-4与S100。结果与创伤组比较,大鼠脑外伤后早期给予高压氧能显著降低脑含水量及AQP-4和caspase-3的表达(P<0．05)。结论早期高压氧治疗能减少大鼠脑外伤后AQP-4和caspase-3的表达,高压氧对创伤性脑损伤的脑保护机制可能与减轻神经胶质细胞介导的细胞性脑水肿、减少神经细胞凋亡有关。
Objective To observe the effects of early hyperbaric oxygen on the expressions of aquaporin-4 and caspase-3 in the brain tissue of rats with brain traumas, and to explore the neuroprotective mechanism of hyperbaric oxygen on brain traumas. Methods Rat brain trauma models were established by the method described by Feeney, and the rats were divided into three groups：sham group（without hitting） , control group（hitting） and HBO group （treated with hyperbaric oxygen 1 h after hitting）. Changes of brain water content （BWC） were measured by the dry-wet weight method. Immunohistochemistry and image analyzing methods were used to determine changes of AQP-g and caspase-3 expressions, and double dyed immunohistochemistry was used to determine AQP-4 and S100 on the 4th day after hitting. Results Compared with the control group, the expressions of AQP-4, caspase-3 and BWC were significantly lower in the HBO group （P 〈 0.05）. Conclusions Early hyperbaric oxygenation could decrease the expression levels of AQP-4 and caspase- 3, and ameliorate cytotoxic brain edema and decrease the apoptosis of neurocytes, which may provide the neuroprotective mechanism against brain traumas.
出处
《中华航海医学与高气压医学杂志》
CAS
CSCD
2006年第4期235-238,共4页
Chinese Journal of Nautical Medicine and Hyperbaric Medicine
