中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
11期
2743-2745
,共3页
预吸氧%血红素氧合酶%一氧化氮%缺氧复氧性脑损伤
預吸氧%血紅素氧閤酶%一氧化氮%缺氧複氧性腦損傷
예흡양%혈홍소양합매%일양화담%결양복양성뇌손상
Preoxygenation%Heme oxygenase%Nitric oxide%Hypoxia reoxygenation injury
目的 观察预吸氧对大鼠缺氧/复氧性脑损伤脑皮质血红素氧合酶-1(HO-1)/一氧化氮(NO)通路的影响.方法 在大鼠脑缺氧复氧前30 min预吸氧30 min,测定大脑皮质HO-1蛋白表达、NO含量和超微结构的变化.结果 大鼠缺氧/复氧后大脑皮质有所损伤,表现为HO-1蛋白表达增加[(0.65±0.18)%增加到(10.50±1.83)%]、NO含量增加[(2.03±0.28) μmol/mg蛋白增加到(5.50 ±0.52) μmol/mg蛋白]和超微结构变化,预吸氧可显著加重这种损伤,HO-1蛋白表达南[(10.50±1.83)%降低到(7.14±1.35)%],NO含量由[(5.50±0.52)μmol/mg蛋白增加到(7.89±0.20)μmol/mg蛋白].结论 预吸氧可加重缺氧复氧性脑损伤,其机制与抑制HO-1蛋白表达及增加NO含量有关.
目的 觀察預吸氧對大鼠缺氧/複氧性腦損傷腦皮質血紅素氧閤酶-1(HO-1)/一氧化氮(NO)通路的影響.方法 在大鼠腦缺氧複氧前30 min預吸氧30 min,測定大腦皮質HO-1蛋白錶達、NO含量和超微結構的變化.結果 大鼠缺氧/複氧後大腦皮質有所損傷,錶現為HO-1蛋白錶達增加[(0.65±0.18)%增加到(10.50±1.83)%]、NO含量增加[(2.03±0.28) μmol/mg蛋白增加到(5.50 ±0.52) μmol/mg蛋白]和超微結構變化,預吸氧可顯著加重這種損傷,HO-1蛋白錶達南[(10.50±1.83)%降低到(7.14±1.35)%],NO含量由[(5.50±0.52)μmol/mg蛋白增加到(7.89±0.20)μmol/mg蛋白].結論 預吸氧可加重缺氧複氧性腦損傷,其機製與抑製HO-1蛋白錶達及增加NO含量有關.
목적 관찰예흡양대대서결양/복양성뇌손상뇌피질혈홍소양합매-1(HO-1)/일양화담(NO)통로적영향.방법 재대서뇌결양복양전30 min예흡양30 min,측정대뇌피질HO-1단백표체、NO함량화초미결구적변화.결과 대서결양/복양후대뇌피질유소손상,표현위HO-1단백표체증가[(0.65±0.18)%증가도(10.50±1.83)%]、NO함량증가[(2.03±0.28) μmol/mg단백증가도(5.50 ±0.52) μmol/mg단백]화초미결구변화,예흡양가현저가중저충손상,HO-1단백표체남[(10.50±1.83)%강저도(7.14±1.35)%],NO함량유[(5.50±0.52)μmol/mg단백증가도(7.89±0.20)μmol/mg단백].결론 예흡양가가중결양복양성뇌손상,기궤제여억제HO-1단백표체급증가NO함량유관.
Objective To investigate the effects of preoxygenation on the heme oxygenase-nitric oxide pathway of the cerebral cortex in rats subjected to hypoxia-reoxygenation injury.Methods At 30 min before hypoxia, preoxygenation was given for 30 min.The heme oxygenase-nitric oxide and ultrastructural changes of the cerebral cortex were examined.Results The cerebral cortex was injured after hypoxia-reoxygen, mainly presented by increased heme oxygenase (HO-1) protein [from (0.65 ± 0.18) % to (10.50 ± 1.83) %] and nitric oxide (NO) content [from (2.03 ± 0.28) μmol/mg protein and (5.50 ±0.52) μ mol/mg protein] , and the ultrastructural changes of the cerebral cortex (P <0.01).Preoxygenation could aggravate the damage of the cerebral cortex [HO-1 protein from (10.50 ± 1.83) % to (7.14 ± 1.35)% , and NO content from (5.50 ±0.52) μmol/mg protein to (7.89 ±0.20) μmol/mg protein].Conclusion Preoxygenation could aggravate the brain injury induced by hypoxia-reoxygenation probably by inhibiting the expression of HO-1 protein and increasing the NO contents.