Abstract:

Objective To investigate the neuroprotective effect of hyperbaric oxygen (HBO) by observing the effect of single 9 hours HBO on apoptosis inducing factor (AIF) and mitochondrial membrane potential (MMPo) in rats with focal cerebral infarction. Methods 108 Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO) using the intraluminal suture method and then were randomly divided into control group and HBO group, with 54 rats in each group. The rats in HBO group started to be exposed to HBO treatment of 0.2 MPa for 9 hours, and the rats in control group breathed air at normal pressure from 3 hours after MCAO. Neurological outcome was measured using Garcia scores, and the number of apoptosis cells, level of AIF expression in mitochondria and nucleus, level of MMPo in ischemic penumbra were measured in both groups at 3th, 13th, 24th and 72th hour after MCAO, and the difference of the above indexes between the two groups were compared. Results (1) Garcia scores: HBO group had a better Garcia score than the control group at 13th hour (P <0.001) and 24th hour (P =0.04) after ischemia. (2) The number of apoptosis cells: HBO group had fewer apoptosis cells than control group at 13th and 24th hour (both P <0.001). (3) The expression of AIF in mitochondria and nucleus: HBO group had higher expression level of AIF in mitochondria than control group at 3th, 24th and 72th hour (all P <0.001), and lower level of AIF in nuclear than control group at the three points (all P <0.001). (4) MMPo: HBO group had higher level of MMPo than control group at the three points (all P <0.001). Conclusions HBO therapy may improve neurological function after MCAO in rats. HBO treatment played a role of neuroprotection by inhibiting cells apoptosis, stabilizing MMPo and inhibiting the transfer of AIF from mitochondria to the nucleus.

Key words: Hyperbaric oxygen; Cerebral infarction; Apoptosis; Apoptosis-inducing factor; Mitochondrial membrane potential

摘要：

目的 观察单次9 h高压氧（hyp erbaric oxygen，HBO）治疗对局灶性脑梗死大鼠凋亡诱导因子 （apoptosis-inducing factor，AIF）、线粒体膜电位（mitochondrial membrane potential，MMPo）的影响，探讨 HBO治疗的神经保护作用。 方法 108只SD大鼠制作永久性大脑中动脉闭塞模型，随机分为对照组和HBO组，每组各54只。造 模成功3 h后，HBO组实行HBO干预，压力0.2 MPa持续9 h，对照组呼吸常压空气。采用Garcia评分评估 大鼠神经功能，比较两组造模后13 h、24 h和72 h神经功能改善情况，并在各时间点检测大鼠缺血半 暗带脑组织凋亡细胞数、线粒体和细胞核AIF表达及MMPo水平。 结果 ①神经功能评分：HBO组13 h（P <0.001）、24 h（P =0.04）神经功能评分改善比对照组更明显。 ②凋亡细胞数：HBO组13 h、24 h凋亡细胞数较对照组更少（均P <0.001）。③AIF在线粒体和细胞核的 表达：13 h、24 h、72 h各时间点HBO组AI F在线粒体的表达均较对照组多（均P <0.001）；各时间点HBO 组AIF在细胞核的表达均较对照组少（均P <0.001）。④MMPo：各时间点HBO组MMPo均高于对照组（均 P <0.001）。 结论 HBO治疗可改善大鼠神经功能，稳定MMPo，抑制AIF由线粒体向细胞核转移可能是其神经保 护作用的机制之一。

关键词: 高压氧; 脑梗死; 凋亡; 凋亡诱导因子; 线粒体膜电位