Geng Fengyang, Ma Yinghua, Xing Tao, Zhuang Xianbo, Zhu Jianxin, Yao Lusu
Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, PR China.
Neuroimmunomodulation. 2016;23(2):122-9. doi: 10.1159/000445689. Epub 2016 May 24.
Neuroinflammation plays an important role in secondary tissue damage after traumatic brain injury (TBI). Recently, the inflammasome-mediated inflammatory pathway has been observed in the inflammatory response of TBI. In this study, we investigated the influence of hyperbaric oxygen therapy (HBOT) on inflammasome activation after TBI.
The experimental mice were randomly divided into 4 groups as follows: sham-operated normobaric air (21% O2 at one absolute atmosphere), HBOT only, TBI + normobaric air and TBI + HBOT. Following the evaluation of motor deficits and brain edema, the expression of inflammasome components and effectors was measured by qRT-PCR and Western blotting. Moreover, alterations in IL-1β, IL-18 and high-mobility group box 1 (HMGB1) were calculated by enzyme-linked immunosorbent assay at each time point after injury.
HBOT improved motor score and reduced brain edema. Furthermore, it suppressed protein expression of inflammasome components and reduced the levels of IL-1β and IL-18, accompanied by the reduction of HMGB1 in brain tissues and serum.
These results suggest that HBOT may alleviate the inflammatory response after TBI by inhibiting the activation of inflammasome signaling.
神经炎症在创伤性脑损伤(TBI)后的继发性组织损伤中起重要作用。最近,在TBI的炎症反应中观察到了炎性小体介导的炎症途径。在本研究中,我们调查了高压氧治疗(HBOT)对TBI后炎性小体激活的影响。
将实验小鼠随机分为4组,如下所示:假手术常压空气组(在一个绝对大气压下21%氧气)、单纯HBOT组、TBI + 常压空气组和TBI + HBOT组。在评估运动功能障碍和脑水肿后,通过qRT-PCR和蛋白质印迹法测量炎性小体成分和效应器的表达。此外,在损伤后的每个时间点,通过酶联免疫吸附测定法计算白细胞介素-1β(IL-1β)、白细胞介素-18(IL-18)和高迁移率族蛋白B1(HMGB1)的变化。
HBOT改善了运动评分并减轻了脑水肿。此外, 它抑制了炎性小体成分的蛋白表达,降低了IL-1β和IL-18水平,同时伴随着脑组织和血清中HMGB1的减少。
这些结果表明,HBOT可能通过抑制炎性小体信号的激活来减轻TBI后的炎症反应。