CAJ | 학술논문

目的观察高压氧治疗对急性创伤性颅脑损伤后海马一氧化氮合酶mRNA(NOS mRNA)表达的影响.方法 42只Sprague-Dawley大鼠按数字表法随机分为6组,每组7只大鼠.采用自由落体打击法制备急性脑创伤模型,伤后1 h、12 h采用0.25 MPa高压氧治疗,伤后6 h、24 h取样海马CA1,应用半定量逆转录聚合酶链反应(RT-PCR)观察诱导性(iNOS)和神经元型一氧化氮合酶(nNOS)mRNA表达量的变化.结果 0.25 MPa高压氧治疗各时间组iNOS mRNA和nNOS mRNA较急性颅脑损伤各时间组显著下降(P<0.01),且高压氧治疗24 h组(0.37±0.12)较急性颅脑损伤24 h组(0.71±0.18)下降更明显(P<0.01),但仍高于高压氧治疗6 h组(0.25±0.10),0.25 MPa常氧高氮各时间组与急性颅脑损伤各时间组无明显改变(P>0.05).结论急性脑创伤后早期nNOS介导毒性作用,iNOS则在晚期介导毒性作用,高压氧治疗可以减少NO的产生,从而在脑创伤后保护海马神经元.
목적 관찰고압양치료대급성창상성로뇌손상후해마일양화담합매mRNA(NOS mRNA)표체적영향.방법 42지Sprague-Dawley대서안수자표법수궤분위6조,매조7지대서.채용자유락체타격법제비급성뇌창상모형,상후1 h、12 h채용0.25 MPa고압양치료,상후6 h、24 h취양해마CA1,응용반정량역전록취합매련반응(RT-PCR)관찰유도성(iNOS)화신경원형일양화담합매(nNOS)mRNA표체량적변화.결과 0.25 MPa고압양치료각시간조iNOS mRNA화nNOS mRNA교급성로뇌손상각시간조현저하강(P<0.01),차고압양치료24 h조(0.37±0.12)교급성로뇌손상24 h조(0.71±0.18)하강경명현(P<0.01),단잉고우고압양치료6 h조(0.25±0.10),0.25 MPa상양고담각시간조여급성로뇌손상각시간조무명현개변(P>0.05).결론 급성뇌창상후조기nNOS개도독성작용,iNOS칙재만기개도독성작용,고압양치료가이감소NO적산생,종이재뇌창상후보호해마신경원.
Objective To investigate the effect of hyperbaric oxygen (HBO) therapy on the expression of nitric oxide synthase (NOS) mRNA in hippocampus following acute traumatic cerebral injury, and also to study the mechanism of HBO on brain injury.Methods Acute traumatic cerebral injury model was established with restricted free fall injury method in Sprague-Dawley rats. HBO therapy at a pressure of 0.25 MPa was administered 1 h or 12 h after brain injury and samples were taken from hippocampus CA1 areas 6 h and 24 h after brain injury respectively. Changes in the expression of mRNA coding for iNOS or nNOS were monitored by using half-quantitative reverse transcription polymerase chain reaction (RT-PCR).Results The expression of iNOS mRNA and nNOS mRNA decreased significantly in the 0.25 MPa HBO therapy group than that of the acute cerebral injury groups (P<0.01). The decrease in the expression of iNOS mRNA and nNOS mRNA was more obvious in the HBOT 24 h group than that of the 24 h acute cerebral injury group (P<0.01). However, their expression was still higher than that of the HBOT 6 h group (0.25±0.10). No significant differences in the expression of iNOS mRNA or nNOS mRNA could be noted, when a comparison was made between the 0.25 MPa NBO group and the acute cerebral injury group (P>0.05).Conclusions Changes in the expression of nNOS at the initial stage of acute traumatic cerebral injury might induce toxication, while the expression of iNOS at the later stage of acute traumatic cerebral injury might induce toxication. HBO therapy seemed to reduce the production of NO and hippocampus neurons might thus be protected, following acute traumatic cerebral injury.