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首页> 外文期刊>Cellular Physiology and Biochemistry >Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke
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Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke

机译：SOCS1-JAK2-STAT3信号通路的抑制赋予缺血性中风大鼠神经保护。

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>Background: The present study aims to investigate the protective effects of the SOCS1-JAK2-STAT3 signaling pathway on neurons in a rat model of ischemic stroke. Methods: Our study was conducted using an ischemic stroke rat model. After the microglia were extracted, 40 neonatal Sprague-Dawley (SD) rats were assigned into the blank, AG490, model and negative control (NC) groups. The neurological function of all the rats was evaluated. Histopathological changes were observed. qRT-PCR and western blotting were applied to measure the expression of genes and proteins in the SOCS1-JAK2-STAT3 signaling pathway and related to apoptosis. The TUNEL assay was conducted to calculate the cellular morphology and apoptosis of neuronal cells. Cell viability was detected using the MTT assay. In addition, immunoassays were used to measure the content of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) as well as the levels of oxidative stress. Results: Compared with the blank group, the model and NC groups showed higher neurological function scoresa€”the cytoplasm of the neurons were cavitated, the organelles were reduced with unclear margins, some of the neurons were necrotic, and apoptosis was increased. In addition, the NC and model groups exhibited decreased cell viability, lower mRNA and protein expression of SOCS1 SOCS3 and bcl-2 and reduced SOD and GSH levels but higher mRNA and protein expression levels of AK2, STAT3,Bax and caspase-3 as well as increased protein expression of P-JAK2, P-STAT3 and activated caspase-3 (c-caspase-3). Moreover, the MDA levels were up-regulated in the NC and model groups. In contrast, opposing trends were found in the AG490 group compared with the NC and model groups. Conclusion: These data demonstrate that inhibiting the SOCS1-JAK2-STAT3 signaling pathway can reduce the loss of nerve function and apoptosis of neuronal cells, which provides a new target for the clinical treatment of ischemic stroke.
机译：> 背景： 本研究旨在研究SOCS1-JAK2-STAT3信号通路对缺血性中风大鼠模型神经元的保护作用。 方法： 我们的研究是使用缺血性中风大鼠模型进行的。提取小胶质细胞后，将40只新生Sprague-Dawley（SD）大鼠分为空白，AG490，模型和阴性对照组（NC）组。评价所有大鼠的神经功能。观察到组织病理学变化。运用qRT-PCR和western blotting检测SOCS1-JAK2-STAT3信号通路中与凋亡相关的基因和蛋白的表达。进行TUNEL测定以计算神经元细胞的细胞形态和凋亡。使用MTT测定法检测细胞活力。此外，免疫测定还用于测量超氧化物歧化酶（SOD），谷胱甘肽（GSH）和丙二醛（MDA）的含量以及氧化应激水平。 结果： 与空白组相比，模型组和NC组的神经功能评分更高：“神经元的细胞质被空化，细胞器减少，边缘不清楚，一些神经元坏死，凋亡增加。此外，NC组和模型组的细胞活力降低，SOCS1 SOCS3和bcl-2的mRNA和蛋白表达降低，SOD和GSH水平降低，但AK2，STAT3，Bax和caspase-3的mRNA和蛋白表达水平也升高。 P-JAK2，P-STAT3和活化的caspase-3（c-caspase-3）蛋白表达增加。此外，NC组和模型组的MDA水平上调。相反，与NC和模型组相比，AG490组发现了相反的趋势。 结论： 这些数据表明，抑制SOCS1-JAK2-STAT3信号通路可以减少神经功能的丧失和神经元细胞的凋亡，为临床提供了新的靶点。缺血性中风的治疗。

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