【摘要】：背景和目的:外傷性腦損傷(TBI)能夠?qū)е聡?yán)重的神經(jīng)功能缺損而且并缺乏有效的治療。炎癥反應(yīng)在TBI后的腦部二次損傷中的關(guān)鍵的病理事件中起到了重要作用,因此,抗炎治療也是針對(duì)TBI的新型治療方向。在近期的研究中,我們已經(jīng)證明了人類白細(xì)胞抗原DRα1結(jié)構(gòu)域連接MOG-35-55肽(DRα1-MOG-35-55)構(gòu)建體在多發(fā)性硬化和缺血性卒中的動(dòng)物模型中減少中樞神經(jīng)系統(tǒng)炎癥和減輕組織損傷的作用。這項(xiàng)研究的目的在于探究DRα1-MOG-35-55治療對(duì)TBI模型小鼠預(yù)后的改善情況。方法:通過液壓打擊在C57BL/6小鼠上構(gòu)建TBI模型。評(píng)估神經(jīng)功能缺損,病灶體積和免疫反應(yīng)來探究DRα1-MOG-35-55治療的療效和神經(jīng)保護(hù)機(jī)制。結(jié)果:DRα1-MOG-35-55構(gòu)建體能夠顯著改善TBI術(shù)后神經(jīng)功能缺損并減小腦部病灶體積。在DRα1-MOG-35-55治療的TBI術(shù)后小鼠體內(nèi),能看到巨噬細(xì)胞浸潤減少,其表達(dá)的CD74和CD86也減少。相反,接受DRα1-MOG-35-55治療后TBI模型小鼠中CD206的表達(dá)增多。DRα1-MOG-35-55治療能夠減少TBI術(shù)后腦組織內(nèi)巨噬細(xì)胞的浸潤。值得注意的是,DRα1-MOG-35-55能夠減少循環(huán)中的CD11b+細(xì)胞的數(shù)量及其表達(dá)CD74的水平。結(jié)論:我們實(shí)驗(yàn)結(jié)果顯示DRα1-MOG-35-55在TBI小鼠模型中的治療可能是有效的。仍然需要進(jìn)一步的研究來證明DRα1-MOG-35-55對(duì)TBI的治療效果。
[Abstract]:Background and objective: traumatic brain injury (TBI) can lead to severe neurological impairment and lack of effective treatment. Inflammation plays an important role in the key pathological events of brain secondary injury after TBI. Therefore, anti-inflammatory therapy is also a new treatment direction for TBI. In recent studies, we have demonstrated the role of human leukocyte antigen Dr 偽 1 domain coupled MOG-35-55 偽 1-MOG-35-55 (Dr 偽 1-MOG-35-55) construction in reducing inflammation and tissue damage in multiple sclerosis and ischemic stroke in animal models. The aim of this study was to explore the improvement of prognosis in TBI model mice treated with Dr 偽 1-MOG-35-55. Methods: TBI model was established on C57BL/6 mice by hydraulic attack. To investigate the therapeutic effect and neuroprotective mechanism of Dr 偽 1-MOG-35-55 by evaluating nerve function defect, focus volume and immune response. Results the ratio Dr 偽 1-MOG-35-55 construction could significantly improve the neurological deficit and reduce the volume of brain focus after TBI. The macrophage infiltration and the expression of CD74 and CD86 in Dr 偽 1-MOG-35-55 treated mice after TBI were decreased. On the contrary, the increase of CD206 expression in TBI model mice after treatment with Dr 偽 1-MOG-35-55. Dr 偽 1-MOG-35-55 treatment could reduce the infiltration of macrophages in brain tissue after TBI. It is worth noting that Dr 偽 1-MOG-35-55 can reduce the number of circulating CD11b cells and the level of CD74 expression. Conclusion: our results suggest that Dr 偽 1-MOG-35-55 may be effective in the treatment of TBI mice. Further research is still needed to demonstrate the efficacy of Dr 偽 1-MOG-35-55 in the treatment of TBI.
【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R651.15

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