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Mechanism of estrogen-mediated intestinal protection following trauma-hemorrhage: p38 MAPK-dependent upregulation of HO-1

机译:创伤性出血后雌激素介导的肠道保护机制:HO-1的p38 MAPK依赖性上调

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摘要

An increasing body of evidence shows that p38 MAPK activation leads to the induction of heme oxygenase (HO)-l (10, 37). HO-1 confers protection against oxidative stress in vivo and in vitro, through antioxidative, antiapoptotic, and anti-inflammatory actions (26, 27). Exogenous administration of HO-1 by gene transfer into rat lung mediates potent anti-inflammatory effects in the lung (27). Moreover, overexpres-sion of HO-1 reduces the expression of adhesion molecules and prevents subsequent leukocyte-endothelial cell interactions and organ damage (32, 38).
机译:越来越多的证据表明p38 MAPK激活导致血红素加氧酶(HO)-1的诱导(10,37)。 HO-1通过抗氧化,抗凋亡和抗炎作用在体内和体外赋予抗氧化应激的保护作用(26,27)。通过基因转移将HO-1外源给药到大鼠肺中,可在肺中发挥有效的抗炎作用(27)。此外,HO-1的过度表达会减少粘附分子的表达,并防止随后的白细胞-内皮细胞相互作用和器官损伤(32、38)。

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