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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Estradiol attenuates the focal cerebral ischemic injury through mTOR/p70S6 kinase signaling pathway.
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Estradiol attenuates the focal cerebral ischemic injury through mTOR/p70S6 kinase signaling pathway.

机译:雌二醇通过mTOR / p70S6激酶信号传导途径减轻局灶性脑缺血损伤。

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摘要

We previously showed that estradiol prevents neuronal cell death through the activation of Akt and its downstream targets Bad and FKHR. This study investigated whether estradiol modulates the survival pathway through other downstream targets of Akt, including mammalian target of rapamycin (mTOR) and p70S6 kinase. It is known that mTOR is a downstream target of Akt and a central regulator of protein synthesis, cell growth, and cell cycle progression. Adult female rats were ovariectomied and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24h after MCAO and infarct volumes were analyzed. We confirmed that estradiol significantly reduces infarct volume and decreases the number of positive cells for TUNEL staining in the cerebral cortex. Brain injury-induced a decrease in phospho-mTOR and phospho-p70S6 kinase. Estradiol prevented the injury-induced decrease in Akt activation and phosphorylation of mTOR and p70S6 kinases, and the subsequent decrease in S6 phosphorylation. Our findings suggest that estradiol plays a potent protective role against brain injury by preventing the injury-induced decrease of mTOR and p70S6 kinase phosphorylation.
机译:我们以前表明,雌二醇可通过激活Akt及其下游靶标Bad和FKHR来防止神经元细胞死亡。这项研究调查了雌二醇是否通过Akt的其他下游靶标(包括哺乳动物雷帕霉素靶标(mTOR)和p70S6激酶)调节生存途径。众所周知,mTOR是Akt的下游靶标,是蛋白质合成,细胞生长和细胞周期进程的中央调节剂。将成年雌性大鼠切除卵巢,并在大脑中动脉闭塞(MCAO)之前用雌二醇治疗。 MCAO 24小时后收集大脑并分析梗死体积。我们证实,雌二醇显着减少了梗塞体积,并减少了大脑皮层中TUNEL染色的阳性细胞数量。脑损伤导致磷酸化mTOR和磷酸化p70S6激酶的减少。雌二醇阻止了损伤诱导的mTOR和p70S6激酶的Akt活化和磷酸化降低,以及随后的S6磷酸化降低。我们的研究结果表明,雌二醇可通过预防损伤诱导的mTOR和p70S6激酶磷酸化水平的降低,对脑损伤起有效的保护作用。

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