Tetrandrine cytotoxicity and its dual effect on oxidative stress-induced apoptosis through modulating cellular redox states in Neuro 2a mouse neuroblastoma cells

Life Sciences ◽  
2002 ◽  
Vol 71 (17) ◽  
pp. 2053-2066 ◽  
Author(s):  
Quanri Jin ◽  
Chulhun Kang ◽  
Yunjo Soh ◽  
Nak Won Sohn ◽  
Juhie Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cells ◽  
Dual Effect ◽  
Cellular Redox ◽  
Redox States ◽  
Mouse Neuroblastoma ◽  
Induced Apoptosis

scholarly journals Ginkgo biloba Prevents Oxidative Stress-Induced Apoptosis Blocking p53 Activation in Neuroblastoma Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 279 ◽  
Author(s):  
Francesco Di Meo ◽  
Rossana Cuciniello ◽  
Sabrina Margarucci ◽  
Paolo Bergamo ◽  
Orsolina Petillo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Ginkgo Biloba ◽  
Apoptotic Cell ◽  
Neuroblastoma Cells ◽  
Apoptotic Cell Death ◽  
Parp Cleavage ◽  
Egb 761 ◽  
Induced Apoptosis

Oxidative stress has been associated to neuronal cell loss in neurodegenerative diseases. Neurons are post-mitotic cells that are very sensitive to oxidative stress—especially considering their limited capacity to be replaced. Therefore, reduction of oxidative stress, and inhibiting apoptosis, will potentially prevent neurodegeneration. In this study, we investigated the neuroprotective effect of Ginkgo biloba extract (EGb 761) against H2O2 induced apoptosis in SK-N-BE neuroblastoma cells. We analysed the molecular signalling pathway involved in the apoptotic cell death. H2O2 induced an increased acetylation of p53 lysine 382, a reduction in mitochondrial membrane potential, an increased BAX/Bcl-2 ratio and consequently increased Poly (ADP-ribose) polymerase (PARP) cleavage. All these effects were blocked by EGb 761 treatment. Thus, EGb 761, acting as intracellular antioxidant, protects neuroblastoma cells against activation of p53 mediated pathway and intrinsic mitochondrial apoptosis. Our results suggest that EGb 761, protecting against oxidative-stress induced apoptotic cell death, could potentially be used as nutraceutical for the prevention and treatment of neurodegenerative diseases.

scholarly journals Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Rui Li ◽  
Wenzhou Liu ◽  
Li Ou ◽  
Feng Gao ◽  
Min Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Inflammatory Factors ◽  
Protective Mechanism ◽  
Human Neuroblastoma ◽  
Induced Apoptosis

Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting H2O2-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated H2O2-induced inflammatory factors, including IL-6, NO, and TNF-α, and alleviated H2O2-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3β signaling pathway. What is more, the PI3K/mTOR/GSK3β pathway participated in the protective mechanism of emodin on H2O2-induced cell damage. Collectively, it suggests that emodin alleviates H2O2-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3β signaling pathway.

scholarly journals Epigallocatechin-3-Gallate Protects Neuro-2a Cells From Sodium Fluoride-Induced Oxidative Damage In Vitro

2020 ◽  
Vol 15 (3) ◽  
pp. 1934578X2091147
Author(s):  
Na Li ◽  
Dongdong Xin ◽  
Hongbo Li ◽  
Yanyan Zhao ◽  
Wei Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Sodium Fluoride ◽  
Neuroblastoma Cells ◽  
Scavenging Activity ◽  
Oxygen Species ◽  
Protective Effects ◽  
Essential Trace Element ◽  
Induced Apoptosis

Fluoride is an essential trace element, but its beneficial range is narrow, and excess fluoride may have negative health effects. The objective of this study was to investigate the potential cytoprotective effects of epigallocatechin-3-gallate (EGCG) in cultured neuro-2a neuroblastoma cells exposed to sodium fluoride (NaF)-induced oxidative stress. Isolated Neuro-2a cells were exposed to increasing concentrations of NaF (0, 1, 2, 4, 6, and 8 mM) for 24 hours to induce oxidative stress. Moreover, to determine the concentration of EGCG necessary for protective effects, we exposed isolated Neuro-2a cells to increasing concentrations of EGCG (0, 0.5, 1, 5, 10, 20, 40, 60, 80, and 100 μg/mL) for 24 and 48 hours. Pretreatment with EGCG at various doses (0, 0.5, 1, 5, 10, 20, and 40 μg/mL) was evaluated in Neuro-2a cells for 24 hours, followed by an NaF (4 mM per culture well) challenge for 24 hours. As shown in this study, EGCG can protect Neuro-2a cells from NaF-induced apoptosis. This effect may be due to the reactive oxygen species scavenging activity of EGCC.

p75NTR activation of NF-κB is involved in PrP106-126-induced apoptosis in mouse neuroblastoma cells

2008 ◽  
Vol 62 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Yu Bai ◽  
Qiang Li ◽  
Jianmin Yang ◽  
Xiangmei Zhou ◽  
Xiaomin Yin ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Mouse Neuroblastoma ◽  
Induced Apoptosis

scholarly journals Dietary polyphenol canolol from rapeseed oil attenuates oxidative stress-induced cell damage through the modulation of the p38 signaling pathway

RSC Advances ◽  
2018 ◽  
Vol 8 (43) ◽  
pp. 24338-24345 ◽  
Author(s):  
Xiaoyang Xia ◽  
Xia Xiang ◽  
Fenghong Huang ◽  
Mingming Zheng ◽  
Renhuai Cong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Rapeseed Oil ◽  
Cell Damage ◽  
Redox Status ◽  
Cellular Redox ◽  
Induced Apoptosis

Canolol extracted from rapeseed oil attenuated oxidative stress-induced apoptosis and cellular redox status imbalance by inhibition of p38 phosphorylation.

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