氧化应激
PI3K/AKT/mTOR通路
活性氧
蛋白激酶B
生物
LY294002型
细胞生物学
细胞凋亡
半胱氨酸蛋白酶3
细胞色素c
信号转导
程序性细胞死亡
生物化学
线粒体
作者
Jihe Kang,Yidian Wang,Xudong Guo,Xuegang He,Wenzhao Liu,Shin-Tson Wu,Zhaoheng Wang,Ai-xin Lin,Xuewen Kang
出处
期刊:Cell Cycle
[Informa]
日期:2022-06-26
卷期号:21 (21): 2268-2282
被引量:3
标识
DOI:10.1080/15384101.2022.2092817
摘要
N-acetylserotonin (NAS) exerts neuroprotective, antioxidant, and anti-apoptotic effects. Oxidative stress and apoptosis are the primary causes of spinal cord injury (SCI). Herein, we explored potential protective effects and mechanisms of NAS in a neuron oxidative damage model in vitro. We established an oxidative damage model in PC12 cells induced by hydrogen peroxide (H2O2) and treated these cells with NAS. NAS enhanced the activity of superoxide dismutase and halted the increase in reactive oxygen species (ROS) and the expression of inducible nitric oxide synthase. Additionally, NAS promoted protein expression of Bcl-2, but inhibited protein expressions of Fas, FADD, cytochrome c, Bax, cleaved caspase-9, and cleaved caspase-3, namely, decreasing protein expression of the Fas and mitochondrial pathways. Furthermore, it reduced the rate of apoptosis and necroptosis-related protein expressions of MLKL and p-MLKL. Moreover, NAS promoted the protein expression of p-PI3K and p-AKT, and the addition of the PI3K inhibitor LY294002 partially attenuated the antioxidant stress and anti-apoptotic effects of NAS in H2O2 stimulated PC12 cells. In conclusion, NAS protected PC12 cells from apoptosis and oxidative stress induced by H2O2 by inhibiting ROS activity and activating the PI3K/AKT signaling pathway.
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