相关实验视频

Updated: Jun 24, 2025

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

在PC12细胞中通过JAK2/STAT3信号通路对BV-2微质介导的亡的作用

Zhao-Da Duan¹, Li-Yang Zheng¹, Qiu-Ye Jia¹

¹Department of Anatomy and Histology/Embryology, Faculty of Basic Medical Sciences, Kunming Medical University, 1168 West Chunrong Road, Kunming, 650500, China.

Scientific reports

|June 11, 2024

概括

斯库特拉林通过调节JAK2/STAT3通路来防止微质诱导的神经元亡. 这项研究揭示了scutellarin.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

微质激活有助于神经元亡.
斯库特拉林显示神经保护的潜力,但其在微质介导的亡的机制是未知的.
这种JAK2/STAT3通路与细胞信号传递和细胞亡有关.

研究的目的:

为了研究skutellarin是否减弱PC12细胞的亡诱导激活的微质细胞.
阐明JAK2/STAT3信号通路在这个过程中的作用.

主要方法:

PC12细胞暴露于来自缺氧-葡萄糖 (OGD) 培养的微质条件介质 (CM).
分析了与亡相关的蛋白质 (Bax,Bcl-2,割裂的卡斯巴酶-3) 和JAK2/STAT3通路蛋白质.
应用了斯库特拉林治疗和JAK2/STAT3抑制剂 (AG490).

主要成果:

OGD-CM增加了PC12细胞亡,增加了Bax和分裂的caspase-3,并降低了Bcl-2.
在OGD-CM中,JAK2/STAT3酸化降低.
斯库特拉林可以逆转这些变化,增加Bcl-2和JAK2/STAT3的酸化.
而AG490治疗降低了斯库特拉林的保护作用.

结论:

斯库特拉林抑制了OGD激活的微质介导的PC12细胞亡.
这种效应通过JAK2/STAT3信号通路进行介导.
斯库特拉林代表了神经退行性疾病的潜在治疗剂,涉及微质激活.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.在JAK2/STAT3信号通道上.微质细胞中的微质细胞这些神经元是神经元.斯库特勒拉里纳是什么意思

更多相关视频

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells

Published on: November 18, 2022

相关概念视频

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...