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xiaowanzi9新蟲(chóng) (正式寫(xiě)手)
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Besides well-described actions on the immune system (see earlier), application of dimethyl fumarate led to effects on endogenous cellular antioxidative pathways involving the transcription factor nuclear (erythroid-derived 2) related factor (Nrf2) [26••]. Nrf2 is a redox-sensitive leucine zipper transcription factor, which contains a domain for interaction with the cytoplasmatic protein kelch-like ECH-associated protein (Keap-1) [27]. In vitro, application of dimethyl fumarate resulted in stabilization of Nrf2, activation of Nrf2-dependent transcriptional activity, and expression of NADPH:quinolone oxidoreductase 1 (NQO1) as a prototypic target gene [28]. Furthermore, application of dimethyl fumarate or MMF involved direct modification of Keap-1 [26••]. On a cellular level, the application of MMF enhanced neuronal survival and protected glial cells against oxidative stress. This action of dimethyl fumarate on cellular resistance to oxidative damage in primary cultures of CNS cells was further substantiated in independent studies [29, 30•] where protective effects were abolished in cells with Nrf2 deficiency [30•]. In vivo, increased levels of Nrf2 were detected in the CNS of dimethyl fumarate treated mice with myelin oligodendrocyte glycoprotein induced EAE. In the very late stage of myelin oligodendrocyte glycoprotein induced EAE, dimethyl fumarate ameliorated the disease course and improved preservation of myelin, axons, and neurons. This effect was not seen in Nrf2-deficient mice [26••]. In summary, activation of Nrf2-dependent antioxidative pathways seems to be an important mechanism of action of dimethyl fumarate. Since oxidative stress may play a major role in the pathogenesis of axonal damage and tissue injury inMS [31], the dimethyl fumarate mediated pharmacological modulation of Nrf2-mediated signaling is an interesting and new therapeutic target not only in experimental models, but also in humans. |
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genhunter
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xiaowanzi9: 金幣+50, 翻譯EPI+1, ★★★★★最佳答案, 謝謝你 2015-05-25 10:38:37
xiaowanzi9: 金幣+50, 翻譯EPI+1, ★★★★★最佳答案, 謝謝你 2015-05-25 10:38:37
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除了已經(jīng)很好描述了的對(duì)免疫系統(tǒng)的效果之外（見(jiàn)前面），反丁烯二酸二甲酯還可通過(guò)細(xì)胞核轉(zhuǎn)錄 因子(紅細(xì)胞來(lái)源的）相關(guān)因子（Nrf2）影響內(nèi)源性的抗氧化通路。Nrf2是一種對(duì)氧化還原敏感的亮氨酸拉鏈轉(zhuǎn)錄因子，它含一個(gè)能與細(xì)胞質(zhì)蛋白Kelch-like ECH-associated protein（keap-1）相互作用域[ 27 ]。在 體外實(shí)驗(yàn)中，使用反丁烯二酸二甲酯導(dǎo)致Nrf2變得穩(wěn)定，從而激活Nrf2依賴(lài)的轉(zhuǎn)錄活性，并表達(dá)它的一個(gè) 典型的靶基因NADPH：喹諾酮類(lèi)藥物的氧化還原酶1（NQO1）[ 28 ]。此外，應(yīng)用反丁烯二酸二甲酯或MMF (估計(jì)是反丁烯二酸單甲酯)還參與keap-1 的直接修飾。在細(xì)胞水平上，使用MMF可以增強(qiáng)神經(jīng)細(xì)胞的存活和保護(hù)神經(jīng)膠質(zhì)細(xì)胞受氧化應(yīng)激(的損傷)。這種反丁烯二酸二甲酯對(duì)原代培養(yǎng)的中樞神經(jīng)細(xì)胞抵抗氧化作用引起的損傷已有獨(dú)立的研究進(jìn)一步證實(shí)[ 29，30 ]，并且保護(hù)作用在沒(méi)有Nrf2表達(dá)的細(xì)胞中不存在•[ 30 ]。在體內(nèi)，在髓鞘少突膠質(zhì)細(xì)胞糖蛋白誘導(dǎo)的EAE模型的小鼠中反丁烯二酸二甲酯處理增加Nrf2的表達(dá)。在髓鞘少突膠質(zhì)細(xì)胞糖蛋白誘導(dǎo)的EAE的晚期，反丁烯二酸二甲酯減緩了病程發(fā)展及改善了對(duì)髓鞘，軸突及神經(jīng)細(xì)胞存活。在Nrf2的基因敲除小鼠內(nèi)沒(méi)有這種效果。 總之，Nrf2依賴(lài)抗氧化通路的激活似乎是一個(gè)反丁烯二酸二甲酯作用的重要機(jī)制作用。由于氧化應(yīng)激可能在軸突損傷和 (MS: multiple sclerosis) 多發(fā)性硬化癥組織損傷中起主要作用[ 31 ]，由富馬酸二甲酯介導(dǎo)的藥理調(diào)控Nrf2介導(dǎo)的信號(hào)轉(zhuǎn)遞是一個(gè)有趣的和新的治療靶點(diǎn)不僅在實(shí)驗(yàn)動(dòng)物模型中，而且在人類(lèi)(治療中也有意義)。 |
2樓2015-05-21 16:08:51
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