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Gnaq Protects PC12 Cells from Oxidative Damage by Activation of Nrf2 and Inhibition of NF-kB.
NeuroMolecular Medicine ( IF 3.5 ) Pub Date : 2020-04-06 , DOI: 10.1007/s12017-020-08598-z
Xin Sun 1, 2 , Guo-Ping Li 3 , Pu Huang 4 , Lu-Gang Wei 5 , Jia-Zhi Guo 6 , Li-Juan Ao 7 , Di Lu 6 , Shao-Chun Chen 1, 7
Affiliation  

Reactive oxygen species (ROS) are continuously produced as byproducts of aerobic metabolism. Oxidative stress (OS) plays an important role in the occurrence of several neurodegenerative diseases as well as aging because of the accumulation of ROS. Gnaq is a member of G protein α subunits. It has been reported that the expression level of Gnaq in the mouse forebrain cortex was significantly decreased with age in our previous study; therefore, we supposed that Gnaq contributes to attenuate the OS. In this study, we generated a Gnaq-overexpression cell using gene recombinant technique and lentivirus transfection technique in a neuron-like PC12 cell, and investigated whether Gnaq had antioxidant effects in PC12 cells treated with H2O2. The viability of cells, concentration of ROS, Nrf2 nuclear translocation, expression of antioxidant enzymes, activation of NF-κB and apoptosis were compared between Gnaq-PC12 cells and Vector-PC12 cells. Results showed that, compared with Vector-PC12 cells, the antioxidative ability of Gnaq-PC12 cells was significantly improved, while the ROS level in Gnaq-PC12 cells was significantly decreased. Nrf2 nuclear translocation was up-regulated and NF-κB nuclear translocation was down-regulated in Gnaq-PC12 cells after H2O2 treatment. The results suggest that Gnaq plays a crucial role in neuroprotection in PC12 cells. A possible mechanism for this would be that the overexpressed Gnaq enhances the antioxidative effect mediated by Nrf2 signal pathway and inhibits the cellular damaging effect through NF-κB signal pathway.

中文翻译:

Gnaq 通过激活 Nrf2 和抑制 NF-kB 保护 PC12 细胞免受氧化损伤。

活性氧 (ROS) 作为有氧代谢的副产品不断产生。由于ROS的积累,氧化应激(OS)在几种神经退行性疾病的发生以及衰老中起着重要作用。Gnaq 是 G 蛋白 α 亚基的成员。在我们之前的研究中已经报道了Gnaq在小鼠前脑皮质中的表达水平随着年龄的增长而显着降低; 因此,我们认为 Gnaq 有助于减弱操作系统。在本研究中,我们利用基因重组技术和慢病毒转染技术在神经元样PC12细胞中生成了Gnaq过表达细胞,并研究了Gnaq对H 2 O 2处理的PC12细胞是否具有抗氧化作用. 比较Gnaq-PC12细胞和Vector-PC12细胞的细胞活力、ROS浓度、Nrf2核转位、抗氧化酶的表达、NF-κB的活化和细胞凋亡。结果表明,与Vector-PC12细胞相比,Gnaq-PC12细胞的抗氧化能力显着提高,而Gnaq-PC12细胞的ROS水平显着降低。H 2 O 2后Gnaq-PC12细胞中Nrf2核转位上调,NF-κB核转位下调治疗。结果表明 Gnaq 在 PC12 细胞的神经保护中起着至关重要的作用。一种可能的机制是过表达的 Gnaq 增强了 Nrf2 信号通路介导的抗氧化作用,并通过 NF-κB 信号通路抑制细胞损伤作用。
更新日期:2020-04-06
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