CAJ | 학술논문

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、7h(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-1αmRNA的表达。结果与中毒组比较，高压氧治疗组的海马组织HIF-1αmRNA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。
목적：탐토고압양(HBO)대급성유궤린중독뇌손상적보호궤제。방법건강웅성SD대서60지，수궤분위정상대조조、중독조、상규치료조화고압양치료조，정상대조조6지，기여3조각18지，건립대서급성유궤린중독뇌손상모형。중독조、상규치료조화고압양치료조분별우건모후1、3、7h(매개시간점6지)하강정맥채혈검측병이철(MDA)적함량화초양화물기화매(SOD)적활성，형광정량PCR검측해마조직HIF-1αmRNA적표체。결과여중독조비교，고압양치료조적해마조직HIF-1αmRNA적표체화혈청MDA함량축점하강(P<0.05)，이혈청SOD활성축점승고(P<0.05)。결론고압양대급성유궤린중독성뇌손상적보호궤제여항양화손상화억제HIF-1α적표체유관，차고압양간예월조월호。
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:con-trol group (n=6), poisoning group (n=18), routine group (n=18) and hyperbaric oxygen group (n=18). All rats were sac-rificed 1 h, 3 h, 7 h after model establishment (six rats at each time point), and the blood samples were taken from in-ferior 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-1αmRNA in the hippocam-pus. Results After the treatment of hyperbaric oxygen, the expression of HIF-1αmRNA 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-1αexpression. The best efficacy will be achieved by the intervention immediately after the brain injury.