摘要
目的探讨高压氧(HBO)对急性有机磷中毒脑损伤的保护机制。方法健康雄性SD大鼠60只,随机分为正常对照组、中毒组、常规治疗组和高压氧治疗组,正常对照组6只,其余3组各18只,建立大鼠急性有机磷中毒脑损伤模型。中毒组、常规治疗组和高压氧治疗组分别于建模后1、3、7 h(每个时间点6只)下腔静脉采血检测丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活性,荧光定量PCR检测海马组织HIF-1α mRNA的表达。结果与中毒组比较,高压氧治疗组的海马组织HIF-1α mRNA的表达和血清MDA含量逐渐下降(P<0.05),而血清SOD活性逐渐升高(P<0.05)。结论高压氧对急性有机磷中毒性脑损伤的保护机制与抗氧化损伤和抑制HIF-1α的表达有关,且高压氧干预越早越好。
Objective To investigate the mechanism of hyperbaric oxygen（HBO） on brain injury caused by acute organophosphate poisoning. Methods Sixty healthy male SD rats were randomly divided into four groups： control group（n=6）, poisoning group（n=18）, routine group（n=18） and hyperbaric oxygen group（n=18）. All rats were sacrificed 1 h, 3 h, 7 h after model establishment（six rats at each time point）, and the blood samples were taken from inferior caval vein, followed by the measurement of malondialdehyde（MDA） content and superoxide dismutase（SOD） activity. The quantitative real time PCR was used to detect the expression of HIF-1α mRNA in the hippocampus. Results After the treatment of hyperbaric oxygen, the expression of HIF-1α mRNA and serum MDA content were significantly lower than that of both in the poisoning group（P〈0.05）. Meanwhile, the serum SOD activity was significantly higher（P〈0.05）. Conclusion The mechanism of hyperbaric oxygen intervention against AOPP-induced brain injury may be the antioxidation and the inhibition of HIF-1α expression. The best efficacy will be achieved by the intervention immediately after the brain injury.
出处
《海南医学》
CAS
2015年第3期319-321,共3页
Hainan Medical Journal
基金
贵州省科技厅资助项目(编号:20092185)
关键词
急性有机磷中毒
脑损伤
缺氧诱导因子-1Α
丙二醛
超氧化物歧化酶
高压氧
Acute organophosphorus poisoning
Brain injury
Hypoxia inducible factor-1alpha
Malondialdehyde
Superoxide dismutase
Hyperbaric oxygen
