本文關鍵詞：tBHQ對顱腦創(chuàng)傷后炎癥反應保護作用的體外研究　出處：《東南大學》2015年碩士論文　論文類型：學位論文

  更多相關文章： 叔丁基對苯二酚 轉錄因子NF-E2相關因子2 顱腦創(chuàng)傷 炎癥反應 核因子-κB

【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作用。動物實驗證實,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,減輕繼發(fā)性腦損傷。本研究擬通過體外實驗,進一步探究tBHQ對顱腦創(chuàng)傷后炎癥反應的保護作用及可能機制。方法：ICR胎鼠培養(yǎng)原代神經(jīng)元細胞,待細胞成熟后,分為三組：(1)對照組；(2)TBI組：(3) TBI+tBHQ組。每組18孔細胞。處理結束24h后Western-Blot技術觀察Nrf2胞漿/核含量,EMSA技術研究核內Nrf2的DNA結合活性、NF-κB的DNA結合活性；Real-timePCR技術定量測定Nrf2-ARE通路下游因子NQO1、HO-1、GST、γGCS的mRNA表達水平；化學發(fā)光法檢測細胞上清GSH、GSSG含量；熒光發(fā)光法檢測細胞上清ROS水平。結果：TBI后細胞核內Nrf2及下游因子NQO1、 HO-1、GST、γGCS表達增加,tBHQ可進一步增加其表達水平(P0.05)。TBI后NF-κB表達明顯增加,細胞上清ROS水平上升,GSH含量下降(P0.05)。對比TBI組,tBHQ可顯著抑制NF-κB的表達,降低細胞上清ROS水平(P0.05)。結論：tBHQ可抑制TBI后繼發(fā)性炎癥反應,從而起到保護作用。其機制可能是通過激活的Nrf2調控細胞內氧化還原反應,進而抑制NF-κB等炎癥信號通路。
[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.

【學位授予單位】：東南大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R651.15

【參考文獻】

相關期刊論文 前3條

1 張秀麗;孫志揚;;大鼠腦損傷后NF-κB的變化及地塞米松干預研究[J];浙江創(chuàng)傷外科;2011年04期

2 唐曉平;王遠傳;彭華;馮凌;漆建;唐文國;茍章洋;余定庸;羅仁國;;顱腦損傷后炎性細胞的變化及其與繼發(fā)性腦損傷的關系[J];中國臨床神經(jīng)外科雜志;2007年07期

3 楊波,關方霞,劉婉華,宋來君;Effect of dexamethasone by local treatment on cerebral edema and serum myelin basic protein after brain injury in rabbits[J];Chinese Journal of Traumatology;2000年04期

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本文編號：1375026