本文關(guān)鍵詞：tBHQ對(duì)顱腦創(chuàng)傷后炎癥反應(yīng)保護(hù)作用的體外研究　出處：《東南大學(xué)》2015年碩士論文　論文類型：學(xué)位論文

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【摘要】：目的：Nrf2通路在顱腦創(chuàng)傷后被激活,在顱腦創(chuàng)傷后具有極為重要的保護(hù)作用。動(dòng)物實(shí)驗(yàn)證實(shí),tBHQ作為Nrf2的激活劑,可以抑制小鼠顱腦創(chuàng)傷后的炎癥反應(yīng),減輕繼發(fā)性腦損傷。本研究擬通過體外實(shí)驗(yàn),進(jìn)一步探究tBHQ對(duì)顱腦創(chuàng)傷后炎癥反應(yīng)的保護(hù)作用及可能機(jī)制。方法：ICR胎鼠培養(yǎng)原代神經(jīng)元細(xì)胞,待細(xì)胞成熟后,分為三組：(1)對(duì)照組；(2)TBI組：(3) TBI+tBHQ組。每組18孔細(xì)胞。處理結(jié)束24h后Western-Blot技術(shù)觀察Nrf2胞漿/核含量,EMSA技術(shù)研究核內(nèi)Nrf2的DNA結(jié)合活性、NF-κB的DNA結(jié)合活性；Real-timePCR技術(shù)定量測定Nrf2-ARE通路下游因子NQO1、HO-1、GST、γGCS的mRNA表達(dá)水平；化學(xué)發(fā)光法檢測細(xì)胞上清GSH、GSSG含量；熒光發(fā)光法檢測細(xì)胞上清ROS水平。結(jié)果：TBI后細(xì)胞核內(nèi)Nrf2及下游因子NQO1、 HO-1、GST、γGCS表達(dá)增加,tBHQ可進(jìn)一步增加其表達(dá)水平(P0.05)。TBI后NF-κB表達(dá)明顯增加,細(xì)胞上清ROS水平上升,GSH含量下降(P0.05)。對(duì)比TBI組,tBHQ可顯著抑制NF-κB的表達(dá),降低細(xì)胞上清ROS水平(P0.05)。結(jié)論：tBHQ可抑制TBI后繼發(fā)性炎癥反應(yīng),從而起到保護(hù)作用。其機(jī)制可能是通過激活的Nrf2調(diào)控細(xì)胞內(nèi)氧化還原反應(yīng),進(jìn)而抑制NF-κB等炎癥信號(hào)通路。
[Abstract]:Objective: Nrf2 pathway is activated in the brain after trauma, plays an important role in protecting the brain injury. Animal experiments confirmed that tBHQ as an activator of Nrf2, can inhibit the inflammatory response in mice after traumatic brain injury, reduce secondary brain injury. This study by in vitro experiments, to further explore the protective effect of tBHQ on the inflammatory response after traumatic brain injury and its possible mechanism. Methods: ICR rat primary cultured neurons, to mature cells, divided into three groups: (1) control group; (2) TBI group: (3) TBI+tBHQ group. Each of the 18 hole cell. Observed Nrf2 cytoplasmic / nuclear Western-Blot content after the end of 24h, EMSA technology to study the nuclear Nrf2 binding activity of DNA, NF- K B DNA binding activity; quantitative Real-timePCR determination of Nrf2-ARE downstream factor NQO1, HO-1, GST, GCS gamma mRNA expression; chemiluminescence detection of cell supernatant containing GSH, GSSG The amount of ROS in the cell supernatant; detection level of fluorescence method. Results: after TBI nucleus Nrf2 and downstream factor NQO1, HO-1, GST, gamma GCS expression increased, tBHQ can further increase the expression level of (P0.05) NF- K B expression was significantly increased after.TBI cell supernatant ROS levels increased, GSH content decreased (P0.05). Compared with TBI group, the expression of tBHQ could significantly inhibit NF- kappa B, reduce the level of ROS cells (P0.05). Conclusion: tBHQ can inhibit the secondary inflammatory reaction after TBI, which play a protective role. The mechanism is probably through the reaction of activated Nrf2 regulation of intracellular redox, and inhibition of NF- K B inflammation signal pathway.

【學(xué)位授予單位】：東南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R651.15

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本文編號(hào)：1375026