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首页> 中文期刊> 《安徽医科大学学报》 >依达拉奉联合高压氧对CO中毒迟发性脑病小鼠血清MDA水平、SOD活性及海马神经元凋亡的影响

依达拉奉联合高压氧对CO中毒迟发性脑病小鼠血清MDA水平、SOD活性及海马神经元凋亡的影响

         
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To investigate the effect of edaravone plus hyperbaric oxygen( HBO ) on MDA level, SOD activity in serum and the apoptosis of hippocampal CA1 area in mice with delayed encephalopathy after acute carbon monoxide poisoning ( DEACMP ). Methods 72 mice were randomly divided into control group, DEACMP group, saline group, HBO group, edaravone group and edaravone plus HBO group( EPH ). The animal model of DEACMP was established by injection of high-dose CO intraperitoneally in mice. The saline group was injected with normal saline through intraperitoneal. HBO group was treated with HBO. Edaravone group was treated with intraperitoneal injection of edaravone. Besides receiving the same HBO treatement as the HBO group, EPH group was also treated with intraperitoneal injection of edaravone. After treatment, serum MDA levels, SOD activity and hippocampal neuron apoptosis of CA1 area were measured in each group. Results ① Compared with control group, serum MDA level was higher and SOD activity was significantly lower in DEACMP group( P < 0. 05 ). Compared with DEACP group, except for the saline group, serum MDA level was lower and SOD activity higher in other treatment groups ( P <0. 05 ). Serum MDA level was lower and SOD activity was higher in EPH group than those in HBO group and edaravone group( P < 0. 05 ); ②There were several apoptotic cells occasionally in hippocampal CA1 area of control group. In addition to saline group, the apoptotic index lower in other treatment groups than that in DEACMP group ( P < 0. 05 ); the apoptotic index of HBO group and edaravone group were higher than in EPH group ( P < 0. 05 ). Conclusion Edaravone plus HBO can reduce MDA levels and increase SOD activity in DEACM, and inhibit the apoptosis of hippocampal CA1 area significantly. The effect of edaravone plus HBO is better than HBO or edaravone treatment.%目的 观察依达拉奉联合高压氧对急性一氧化碳中毒迟发性脑病小鼠血清丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性及海马CA1区神经元凋亡的影响.方法 将72只小鼠随机分为对照组、迟发性脑病(DEACMP)组、生理盐水组、高压氧(HBO)组、依达拉奉组及联合治疗组.使用腹腔注射一氧化碳的方法 制备一氧化碳中毒迟发性脑病的模型.染毒后15~28 d生理盐水组腹腔注射生理盐水,HBO组行HBO治疗,依达拉奉组腹腔注射依达拉奉,联合治疗组行HBO加腹腔注射依达拉奉治疗.治疗结束后每组分别检测血清MDA水平、SOD活性及海马CA1区神经元凋亡情况.结果 ①血清MDA、SOD测定结果:DEACMP组小鼠血清MDA含量高于对照组,SOD活性低于对照组(P<0.05);与DEACMP组相比,除生理盐水组外,余治疗组血清MDA含量降低,SOD活性升高,差异有统计学意义(P<0.05);HBO组及依达拉奉组MDA含量高于联合治疗组,而SOD活性均低于联合治疗组,差异有统计学意义(P<0.05);②海马CA1区神经元凋亡:对照组海马CA1区偶见少量凋亡细胞,除生理盐水组外的各治疗组凋亡指数均低于DEACMP组(P<0.05);HBO组及依达拉奉组凋亡指数高于联合治疗组(P<0.05).结论 依达拉奉与HBO联合治疗可以有效降低急性一氧化碳中毒迟发性脑病小鼠血清MDA水平、提高SOD活性,并可以显著抑制海马CA1区神经元凋亡发生,效果优于单纯HBO或者依达拉奉治疗.

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