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首页> 外文期刊>The European Journal of Neuroscience >Role of heme oxygenase-1 protein in the neuroprotective effects of cyclopentenone prostaglandin derivatives under oxidative stress.
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Role of heme oxygenase-1 protein in the neuroprotective effects of cyclopentenone prostaglandin derivatives under oxidative stress.

机译：血红素加氧酶-1蛋白在氧化应激下环戊烯酮前列腺素衍生物的神经保护作用中的作用。

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Previously we found that some cyclopenteone prostaglandin derivatives (PGs), referred to as neurite outgrowth-promoting PGs (NEPPs), have dual biological activities of promoting neurite outgrowth and preventing neuronal death [Satoh et al. (2000) J. Neurochem., 75, 1092-1102; Satoh et al. (2001) J. Neurochem., 77, 50-62; Satoh et al. (2002) In Kikuchi, II. (ed.), Strategenic Medical Science Against Brain Attack. Springer-Verlag, Tokyo, pp. 78-93]. To investigate possible cellular mechanisms of the neuroprotective effects, we performed oligo hybridization-based DNA array analysis with mRNA isolated from HT22, a cell line that originated from a mouse hippocampal neuron. Several transcripts up-regulated by NEPP11 were identified. Because heme oxygenase 1 (HO-1) mRNA was the most prominently induced and was earlier reported to protect neuronal and non-neuronal cells against oxidative stress, we focused on it as a possible candidate responsible for the neuroprotective effects. We found NEPP11 to induce HO-1protein (32 kDa) in HT22 cells in both the presence and the absence of glutamate, whereas non-neuroprotective prostaglandins (PGs) Delta12-PGJ2 or PGA2 did not. Overexpression of HO-1-green fluorescence protein (GFP) fusion protein significantly protected HT22 cells against oxidative glutamate toxicity, whereas that of GFP alone did not. Furthermore, biliverdin and bilirubin, products of HO-1 enzymatic activity on heme, protected HT22 cells from oxidative glutamate toxicity. These results, together with our previous results, suggest that NEPP11 activates the expression of HO-1 and that HO-1 produces biliverdin and bilirubin, which result in the inhibition of neuronal death induced by oxidative stress. NEPP11 is the first molecular probe reported to have a neuroprotective action through induction of HO-1 in neuronal cells.
机译：先前我们发现一些环戊烯前列腺素衍生物（PGs），称为神经突增生PG（NEPPs），具有促进神经突增生和防止神经元死亡的双重生物学活性[Satoh等。 （2000）J.Neurochem。，75，1092-1102;佐藤等。 （2001）J. Neurochem。，77，50-62;佐藤等。 （2002）在菊池，II。 （编），《抗脑攻击的战略医学》。 Springer-Verlag，东京，第78-93页]。为了研究神经保护作用的可能细胞机制，我们用分离自HT22的mRNA进行了基于寡核苷酸杂交的DNA阵列分析，HT22是一种源自小鼠海马神经元的细胞系。鉴定了由NEPP11上调的几个转录物。由于血红素加氧酶1（HO-1）mRNA的诱导最显着，并且据报道较早时可以保护神经元和非神经元细胞免受氧化应激，因此我们将其重点放在可能引起神经保护作用的候选基因上。我们发现NEPP11在存在和不存在谷氨酸的情况下均可在HT22细胞中诱导HO-1蛋白（32 kDa），而非神经保护性前列腺素（PGs）Delta12-PGJ2或PGA2则不。 HO-1-绿色荧光蛋白（GFP）融合蛋白的过表达显着保护了HT22细胞免受谷氨酸的氧化毒性，而单独使用GFP则没有。此外，HO-1对血红素具有酶促活性的产物biliverdin和bilirubin保护HT22细胞免受谷氨酸的氧化毒性。这些结果以及我们以前的结果表明，NEPP11激活HO-1的表达，而HO-1产生biliverdin和胆红素，从而抑制了氧化应激诱导的神经元死亡。 NEPP11是第一种据报道通过在神经元细胞中诱导HO-1具有神经保护作用的分子探针。

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