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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >INTERLEUKIN-10 MEDIATES THE NEUROPROTECTION OF HYPERBARIC OXYGEN THERAPY AGAINST TRAUMATIC BRAIN INJURY IN MICE
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INTERLEUKIN-10 MEDIATES THE NEUROPROTECTION OF HYPERBARIC OXYGEN THERAPY AGAINST TRAUMATIC BRAIN INJURY IN MICE

机译：白细胞介素-10介导对创伤性脑损伤的高氧氧疗神经保护。

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摘要

The aim of present study was to elucidate the role of lnterleukin-10 (IL-10) in the neuroprotection of hyperbaric oxygen (HBO) against traumatic brain injury (TBI) in mice. The TBI in mice was induced by controlled cortical impact (CCI). HBO was given for 1 h at 2.0 absolute atmosphere (ATA) in 100% O_2- HBO enhanced the serumal and cerebral IL-10 protein levels in both sham-operated and TBI mice. HBO therapy after TBI reduced lesion volume, attenuated cerebral edema, improved neurological status including motor and cognitive function, inhibited apoptosis evidenced by decreased ratio of cleaved caspase-3 (C3) to pro-C3 and Bax expression and increased bcl-2 expression, and attenuated inflammation marked by reduced expression of IL-1p, IL-6, macrophage inflammatory protein-2 (MIP-2), and mono-cyte chemoattractant protein-1 (MCP-1) and activity of matrix metalloproteinase-9 (MMP9). In addition, HBO after TBI improved the blood-brain barrier, and upregulated the expression of tight junction proteins including zonula occlu-dens-1 (ZO-1) and claudin-5. IL-10 deficiency aggravated TBI-induced damage in the brain and abrogated the beneficial effects of HBO on neuroinflammation, apoptosis, and edema after TBI. IL-10 deficiency itself had no significant effect on brain water content and neurological status. In conclusion, IL-10 played an important role in the neuroprotection of HBO therapy against TBI in mice.
机译：本研究的目的是阐明白介素10（IL-10）在高压氧（HBO）对小鼠颅脑损伤（TBI）的神经保护中的作用。小鼠的TBI是通过控制皮层撞击（CCI）诱导的。在100％O_2中于2.0绝对大气（ATA）下给予HBO 1小时-HBO增强了假手术和TBI小鼠的血清和脑IL-10蛋白水平。 TBI后的HBO治疗减少了病变体积，减轻了脑水肿，改善了包括运动和认知功能在内的神经系统状态，抑制了凋亡，这由裂解的caspase-3（C3）与pro-C3和Bax的表达比例降低以及bcl-2的表达升高证明，并且IL-1p，IL-6，巨噬细胞炎性蛋白2（MIP-2）和单细胞趋化蛋白1（MCP-1）的表达降低以及基质金属蛋白酶9（MMP9）的活性降低，从而减轻炎症。此外，TBI后的HBO改善了血脑屏障，并上调了紧密连接蛋白的表达，包括紧密带小结1（ZO-1）和claudin-5。 IL-10缺乏症加重了TBI引起的脑损伤，并废除了HBO对TBI后神经炎症，凋亡和水肿的有益作用。 IL-10缺乏症本身对脑含水量和神经系统状态无明显影响。总之，IL-10在HBO对抗TBI小鼠的神经保护中起着重要作用。

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