Xylocoside G Reduces Amyloid-β Induced Neurotoxicity by Inhibiting NF-κB Signaling Pathway in Neuronal Cells

2012 ◽  
Vol 30 (2) ◽  
pp. 263-275 ◽  
Author(s):  
Yan Yu ◽  
Liang Zhou ◽  
Miao Sun ◽  
Ting Zhou ◽  
Kaiyin Zhong ◽  
...  
2012 ◽  
Vol 7 (Suppl 1) ◽  
pp. S28 ◽  
Author(s):  
Xuehua Wu ◽  
Yan Yu ◽  
Liang Zhou ◽  
Hecheng Wang ◽  
Huan Yang ◽  
...  

2018 ◽  
Vol 32 (12) ◽  
pp. 6737-6759 ◽  
Author(s):  
Xiang Xu ◽  
Enping Huang ◽  
Baoying Luo ◽  
Dunpeng Cai ◽  
Xu Zhao ◽  
...  

2021 ◽  
Vol 22 (5) ◽  
pp. 2274
Author(s):  
Hyun-Su Lee ◽  
Eun-Nam Kim ◽  
Gil-Saeng Jeong

Methamphetamine (METH) is a highly addictive drug that induces irreversible damage to neuronal cells and pathological malfunction in the brain. Aromadendrin, isolated from the flowers of Chionanthus retusus, has been shown to have anti-inflammatory or anti-tumor activity. Nevertheless, it has been reported that METH exacerbates neurotoxicity by inducing endoplasmic reticulum (ER) stress via the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in neuronal cells. There is little evidence that aromadendrin protects cells from neurotoxicity induced by METH. In this study, we found that aromadendrin partially suppressed the METH-induced cell death in SH-SY5y cells without causing cytotoxicity. Aromadendrin regulated METH-induced ER stress by preserving the phosphorylation of the PI3K/Akt/mTOR signaling pathway in METH-exposed SH-SY5y cells. In addition, aromadendrin mitigated METH-induced autophagic and the apoptotic pathways in METH-exposed SH-SY5y cells. Mechanistic studies revealed that pre-treatment with aromadendrin restored the expression of anti-apoptotic proteins in METH-exposed conditions. The inhibitor assay confirmed that aromadendrin-mediated restoration of mTOR phosphorylation protected cells from autophagy and apoptosis in METH-exposed cells. Therefore, these findings suggest that aromadendrin relatively has a protective effect on SH-SY5y cells against autophagy and apoptosis induced by METH via regulation of ER stress and the PI3K/Akt/mTOR signaling pathway.


2001 ◽  
pp. 229-232
Author(s):  
Masamichi Nakai ◽  
Satoshi Tanimukai ◽  
Keiko Yagi ◽  
Naoaki Saito ◽  
Hiroshi Hasegawa ◽  
...  

RSC Advances ◽  
2020 ◽  
Vol 10 (28) ◽  
pp. 16593-16606 ◽  
Author(s):  
Naw Hser Gay ◽  
Wilasinee Suwanjang ◽  
Waralee Ruankham ◽  
Napat Songtawee ◽  
Prapimpun Wongchitrat ◽  
...  

Neuronal cells exposed to H2O2 may undergo increase ROS, reduction in cell viability and cell death. Butein, isoliquiritigenin, and scopoletin ameliorated H2O2-induced neurotoxicity by reducing ROS, balancing antioxidants and activating SIRT1-FoxO3a-ADAM10 pathway.


2019 ◽  
Vol 72 (1) ◽  
pp. 97-109 ◽  
Author(s):  
Qin Cao ◽  
Tian Meng ◽  
Jianhui Man ◽  
Dong Peng ◽  
Hongxia Chen ◽  
...  

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