炎症体
创伤性脑损伤
神经炎症
HMGB1
医学
炎症
水肿
药理学
内科学
精神科
作者
Fengyang Geng,Yinghua Ma,Tao Xing,Xianbo Zhuang,Jianxin Zhu,Lusu Yao
摘要
<b><i>Objective:</i></b> 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. <b><i>Methods:</i></b> The experimental mice were randomly divided into 4 groups as follows: sham-operated normobaric air (21% O<sub>2</sub> 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. <b><i>Results:</i></b> 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. <b><i>Conclusion:</i></b> These results suggest that HBOT may alleviate the inflammatory response after TBI by inhibiting the activation of inflammasome signaling.
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