高压氧处理对大鼠大脑缺血缺氧再灌注损伤保护作用的研究

The study on the protective effect of hyperbaric oxygen on cerebral ischemia hypoxia reperfusion injury in rats

目的研究高压氧处理对大鼠大脑组织缺血缺氧再灌注损伤的保护作用及其可能机制。方法雄性SD大鼠32只随机分成假手术对照组(n=4)、线栓模型组(n=14)和高压氧治疗组(n=14)。Bederson方法评定大鼠神经功能;TTC染色测量大鼠脑组织梗死体积;免疫组化染色测定大鼠脑组织中TNF-α和NF-κB p65表达量;Western blot检测大鼠脑组织中NF-κB p65含量。结果与假手术对照组大鼠比较,线栓模型组和高压氧治疗组大鼠的神经功能均有损害,并出现明显的局灶性梗死(P<0.05);与线栓模型组比较,高压氧治疗组大鼠神经功能损害较轻,梗死面积也较小(P<0.01)。与假手术对照组大鼠比较,线栓模型组和高压氧治疗组大鼠大脑组织TNF-α和NF-κB p65表达量(IOD值)均较低(P<0.01),但高压氧治疗组降低更为明显(P<0.01)。Western blot测定显示,经高压氧处理7d后,大鼠大脑额叶皮层内NF-κB p65相对表达量明显降低(P<0.01)。结论高压氧治疗可能通过下调TNF-α和NF-κB p65表达减少实验性缺血缺氧再灌注大鼠脑梗塞体积,改善大鼠神经功能缺损。

Objective To study the protective effect of hyperbaric oxygen on cerebral ischemia reperfusion injury in rats and its possible mechanism.Methods 32 male SD rats were randomly divided into sham operation group(n=4),model group(n=14)and hyperbaric oxygen treatment group(n=14).A modified Zea-Longa method was used to establish a rat model of ischemia.The infarct volume was measured by TTC staining.The expressions of TNF-αand NF-κB p65 in rat brain were determined by immunohistochemical staining.The expression of NF-κB p65 in rat brain was determined by Western blot.Results Compared with the sham operation group,the nerve function of rats in the model group and the hyperbaric oxygen treatment group were damaged,and obvious focal infarction appeared(P<0.05).Compared with the model group,the nerve function damage and infarct area of hyperbaric oxygen treatment group were lighter(P<0.01).Compared with the sham operation group,the expression of TNF-αand NF-κB p65(IOD value)in the brain tissue of rats in the model group and the hyperbaric oxygen treatment group were lower(P<0.01),but the decrease was more obvious in the hyperbaric oxygen treatment group(P<0.01).After 7 days of hyperbaric oxygen treatment,the relative expression of NF-κb p65 in the frontal cortex of rats was significantly decreased(P<0.01).Conclusion The hyperbaric oxygen therapy may reduce the cerebral infarct volume and improve the neurological deficit in rats by down-regulating the expression of TNF-αand NF-κB p65.