高压氧对大鼠急性脑梗死的治疗作用及其机制

Therapeutic effect of hyperbaric oxygen on acute cerebral infarction in rats and its mechanism

目的观察高压氧(HBO)对大鼠急性脑梗死的治疗作用,并探讨其机制。方法 150只SD大鼠随机分为治疗组(60只)、模型组(60只)、对照组(30只),模型组与治疗组大鼠从颈外动脉处逆行穿刺插管注入0. 3 m L栓塞液制备急性脑梗死模型,对照组注入同体积的生理盐水。制模后治疗组高压氧治疗1、3、7、14、21、28 d(分别计为T1、T2、T3、T4、T5、T6),1次/d。比较各组不同时点大鼠神经功能评分、脑组织含水量、脑梗死体积、缺氧诱导因子-1α(HIF-1α)阳性神经元数、HIF-1α mRNA相对表达量。结果与对照组比较,治疗组和模型组T1~T6神经功能评分增加(P均<0. 05);与模型组比较,治疗组T1~T6神经功能评分减少(P均<0. 05)。与对照组比较,治疗组和模型组T1~T4脑组织含水量升高(P均<0. 05);与模型组比较,治疗组T1~T3脑组织含水量降低(P均<0. 05)。与对照组比较,治疗组和模型组T1~T6脑梗死体积增加(P均<0. 05);与模型组比较,治疗组T2~T6脑梗死体积减少(P均<0. 05)。与对照组比较,治疗组和模型组T1~T6HIF-1α阳性神经元数增加(P均<0. 05);与模型组比较,T1~T3HIF-1α阳性神经元数增加(P均<0. 05)。与对照组比较,治疗组和模型组T1~T6脑梗死区域HIF-1α mRNA相对表达量增加(P均<0. 05);与模型组比较,治疗组T1~T3脑梗死区域HIF-1α mRNA相对表达量增加(P均<0. 05)。结论 HBO对大鼠急性脑梗死有治疗作用,机制可能与其可促进皮质和海马HIF-1α过度表达有关。

Objective To observe the therapeutic effect of hyperbaric oxygen( HBO) on acute cerebral infarction in rats and to explore its mechanism. Methods Totally 150 SD rats were randomly divided into the treatment group( n = 60),model group( n = 60),and control group( n = 30). Rats in the model group and the treatment group were injected with 0. 3 m L embolization solution from the external carotid artery to establish the acute cerebral infarction models,and the mice in the control group were given an equal volume of normal saline. Hyperbaric oxygen therapy was performed in the treatment group on day 1,3,7,14,21 and 28( T1,T2,T3,T4,T5 and T6,respectively),once a day. The neural function score,brain water content,infarct volume,number of HIF-1 α positive neurons and relative expression of HIF-1α mRNA at different time points were compared among the three groups. Results Compared with the control group,the score of nerve function at T1-T6 and the water content of brain tissues at T1-T4 increased in the treatment group and model group( all P < 0. 05). Compared with the model group,the score of nerve function decreased in the treatment group at T1-T6( all P <0.05),and the water content of brain tissues decreased at T1-T3( all P <0.05). Compared with the control group,the volume of cerebral infarction increased at T1-T6( all P <0. 05),and the number of HIF-1α positive neurons increased( all P < 0. 05). Compared with the model group,the volume of cerebral infarction decreased at T2-T6( all P <0.05),and the number of HIF-1α positive neurons increased at T1-T6( all P <0.05). The relative expression of HIF-1 α mRNA in the treatment group and model group were higher than those in the control group( all P< 0. 05),which in the treatment group were higher than those in the model group at T1-T3( all P <0.05). Conclusion HBO has therapeutic effect on acute cerebral infarction in rats,and the mechanism may be related to the over-expression of HIF-1α in cortex and hippocampus.