Heme oxygenase-I exacerbates early brain injury after intracerebral haemorrhage
Heme oxygenase-I exacerbates early brain injury after intracerebral haemorrhage
复制标题
DOI：
10.1093/brain/awm095
复制
发表时间：
2007-06-01
期刊：
影响因子：
14.5
通讯作者：
Dore, Sylvain
中科院分区：
文献类型：
--
作者：
Wang, Jian;Dore, Sylvain
由于血红素氧合酶（HO）是血液中促氧化剂氯化血红素/血红素降解的限速酶，在此我们研究了诱导型HO-Ⅰ对脑出血（ICH）引起的早期脑损伤的作用。我们发现，在诱导ICH后，IHO-I蛋白在ICH周围区域高度可检测，主要在小胶质细胞/巨噬细胞和内皮细胞中。值得注意的是，在ICH后24和72小时，IH 10- I敲除（HO-I-/-）小鼠的损伤体积显著小于野生型对照组。尽管脑含水量没有明显差异，但HO-1-/-小鼠的保护作用与ICH诱导的白细胞浸润、小胶质细胞/巨噬细胞活化和自由基水平的显著降低有关。这些数据揭示了HO-1在ICH后早期脑损伤中的作用，这是以前未认识到的。因此，HO-1信号转导的调节应在临床环境中进一步评估。特别是对于出血状态。
Because heme oxygenase (HO) is the rate limiting enzyme in the degradation of the pro-oxidant hemin/heme from blood, here we investigated the contribution of the inducible HO-I to early brain injury produced by intracerebral haemorrhage (ICH). We found that after induction of ICH, IHO- I proteins were highly detectable in the peri-ICH region predominantly in microglia/macrophages and endlothelial cells. Remarkably, the injury volume was significantly smaller in IH10- I knockout (HO-I-/-) mice than in wild-type controls 24 and 72 h after ICH. Although the brain water content did not appear to be significantly different, the protection in HO-I-/- mice was associated with a marked reduction in ICH-induced leucocyte infiltration, microglia/macrophage activation and free radical levels.These data reveal a previously unrecognized role of HO- I in early brain injury after ICH.Thus, modulation of HO-I signalling should be assessed further in clinical settings, especially for haemorrhagic states.