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创伤性脑损伤后,高压氧治疗可抑制小胶质细胞的激活。

Microglial activation induced by traumatic brain injury is suppressed by postinjury treatment with hyperbaric oxygen therapy.

机构信息

Department of Neurosurgery, Chi-Mei Medical Center, Tainan, Taiwan.

出版信息

J Surg Res. 2013 Oct;184(2):1076-84. doi: 10.1016/j.jss.2013.04.070. Epub 2013 May 21.

DOI:10.1016/j.jss.2013.04.070
PMID:23726237
Abstract

BACKGROUND

The mechanisms underlying the protective effects of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) are unclear. TBI initiates a neuroinflammatory cascade characterized by activation of microglia and increased production of proinflammatory cytokines. In this study, we attempted to ascertain whether the occurrence of neuroinflammation exhibited during TBI can be reduced by HBO.

METHODS

TBI was produced by the fluid percussion technique in rats. HBO (100% O2 at 2.0 absolute atmospheres) was then used at 1 h (HBO I) or 8 h (HBO II) after TBI. Neurobehavior was evaluated by the inclined plane test on the 72 h after TBI and then the rats were killed. The infarction area was evaluated by Triphenyltetrazolium chloride. Immunofluorescence staining was used to evaluate neuronal apoptosis (TUNEL + NeuN), microglial cell aggregation count (OX42 + DAPI), and tumor necrosis factor-alpha (TNF-α) expression in microglia cell (OX42 + TNF-α).

RESULTS

The maximum grasp angle in the inclined plane test and cerebral infarction of the rats after TBI were significantly attenuated by HBO therapy regardless of whether the rats were treated with HBO 1 or 8 h after TBI compared with the controls. TBI-induced microglial activation, TNF-α expression, and neuronal apoptosis were also significantly reduced by HBO therapy.

CONCLUSIONS

Our results demonstrate that treatment of TBI during the acute phase of injury can attenuate microgliosis and proinflammatory cytokine TNF-α expression resulting in a neuroprotective effect. Even treating TBI with HBO after 8 h had a therapeutic effect.

摘要

背景

高压氧(HBO)治疗对创伤性脑损伤(TBI)的保护作用的机制尚不清楚。TBI 会引发神经炎症级联反应,其特征是小胶质细胞激活和促炎细胞因子产生增加。在这项研究中,我们试图确定 TBI 期间发生的神经炎症是否可以通过 HBO 来减轻。

方法

通过液压冲击技术在大鼠中产生 TBI。然后,在 TBI 后 1 小时(HBO I)或 8 小时(HBO II)使用 HBO。在 TBI 后 72 小时通过斜面试验评估神经行为,然后处死大鼠。通过氯化三苯基四氮唑评估梗死面积。免疫荧光染色用于评估神经元凋亡(TUNEL + NeuN)、小胶质细胞聚集计数(OX42 + DAPI)和小胶质细胞中肿瘤坏死因子-α(TNF-α)的表达(OX42 + TNF-α)。

结果

与对照组相比,无论大鼠在 TBI 后 1 小时还是 8 小时接受 HBO 治疗,TBI 后大鼠在斜面试验中的最大抓握角度和脑梗死均明显减轻。HBO 治疗还显著减轻了 TBI 诱导的小胶质细胞激活、TNF-α表达和神经元凋亡。

结论

我们的结果表明,在损伤的急性期治疗 TBI 可以减轻小胶质细胞增生和促炎细胞因子 TNF-α的表达,从而产生神经保护作用。即使在 TBI 后 8 小时用 HBO 治疗也有治疗效果。

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