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首页> 外文期刊>The European Journal of Neuroscience >Neuroprotection by estrogen via extracellular signal-regulated kinase against quinolinic acid-induced cell death in the rat hippocampus.
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Neuroprotection by estrogen via extracellular signal-regulated kinase against quinolinic acid-induced cell death in the rat hippocampus.

机译：雌激素通过细胞外信号调节激酶对喹啉酸诱导的大鼠海马细胞死亡的神经保护作用。

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摘要

Extracellular signal-regulated kinase (ERK) belongs to the family of mitogen-activated protein kinases (MAPKs), which are serine-threonine kinases activated by phosphorylation in response to a variety of mitogenic signals. We previously reported that 17 beta-estradiol rapidly activates ERK in the rat hippocampus. However, the physiological role of this rapid activation of ERK by estrogen in vivo has not yet been elucidated. This study investigated whether ERK may participate in mediating the neuroprotective effects of estrogen against quinolinic acid (QA) toxicity in the rat hippocampus in vivo. Injection of QA into the hippocampi of male rats produced a loss of Nissl-stained neurons in the CA1 after 24 h. Prior administration of 17 beta-estradiol (50 pmol/animal) to the ventricles prevented the QA-induced decrease in Nissl-stained neurons. Pretreatment with U0126, an inhibitor of MAPK/ERK kinase, inhibited the rapid activation of ERK by 17 beta-estradiol in the rat hippocampus. Moreover, the neuroprotective effects of 17beta-estradiol against QA toxicity were blocked by the pretreatment with U0126. U0126 alone did not produce a loss of neurons. These results indicate that ERK mediates estrogen neuroprotection after QA toxicity in the rat hippocampus.
机译：细胞外信号调节激酶（ERK）属于丝裂原激活的蛋白激酶（MAPK）家族，它们是丝氨酸-苏氨酸激酶，可通过磷酸化响应多种促有丝分裂信号而被激活。我们先前曾报道17β-雌二醇迅速激活大鼠海马中的ERK。然而，尚未阐明体内雌激素快速激活ERK的生理学作用。这项研究调查了ERK是否可能参与介导雌激素对大鼠海马体内喹啉酸（QA）毒性的神经保护作用。在24小时后，将QA注入雄性大鼠海马体会在CA1中丢失Nissl染色的神经元。事先给脑室施用17β-雌二醇（50 pmol /动物）可防止QA诱导的Nissl染色神经元减少。用MAPK / ERK激酶抑制剂U0126预处理可抑制大鼠海马中17β-雌二醇对ERK的快速激活。此外，U0126预处理阻断了17β-雌二醇对QA毒性的神经保护作用。仅U0126不会产生神经元的丢失。这些结果表明在大鼠海马QA毒性后，ERK介导雌激素神经保护作用。

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