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Cancer: Neuroblastoma
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Total 79 results found since Jan 2013.
Curcumin protects neural cells against ischemic injury in N2a cells and mouse brain with ischemic stroke
ConclusionCurcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.
Curcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, w...
Source: Brain and Behavior - December 1, 2017 Category: Neurology Authors: Cai ‐Jun Xie, Ai‐Ping Gu, Jun Cai, Yi Wu, Rui‐Cong Chen Tags: ORIGINAL RESEARCH Source Type: research
Upregulation of miR-219a-5p Decreases Cerebral Ischemia/Reperfusion Injury In Vitro by Targeting Pde4d
In this study, we explored the neuroprotective effects of miR-219a-5p on brain using an in vitro ischemia model (mouse neuroblastoma N2a cells treated with oxyglucose deprivation and reperfusion), and in vivo cerebral I/R model in mice.
Source: Journal of Stroke and Cerebrovascular Diseases - April 1, 2020 Category: Neurology Authors: Min-Yi Lu, Jin-Rong Wu, Rui-Bing Liang, Yu-Peng Wang, You-Cai Zhu, Zi-Ting Ma, Hao Zhang, Jie Zan, Wen Tan Source Type: research
The Effects of Intelectin-1 on Antioxidant and Angiogenesis in HUVECs Exposed to Oxygen Glucose Deprivation
Conclusion: These results suggest intelectin-1 promotes angiogenesis, inhibits oxidative stress and reduces apoptosis by stimulating the Akt-eNOS signaling pathway in response to ischemia in vitro.
Introduction
Stroke is a main reason of human neurological disability, ischemic stroke (IS) accounts for almost 80–90% of all strokes. IS occurs after a cerebral blood flow disruption, leading to cellular death and tissue damage by restricting glucose and oxygen supplies (1). Ischemic vascular diseases cause substantial vascular valve and vascular endothelial cell injuries, eventually damaging the surrounding tis...
Source: Frontiers in Neurology - April 15, 2019 Category: Neurology Source Type: research
Humanin analogue, S14G-humanin, has neuroprotective effects against oxygen glucose deprivation/reoxygenation by reactivating Jak2/Stat3 signaling through the PI3K/AKT pathway.
Authors: Gao GS, Li Y, Zhai H, Bi JW, Zhang FS, Zhang XY, Fan SH
Abstract
Stroke, characterized by a disruption of blood supply to the brain, is a major cause of morbidity and mortality worldwide. Although humanin, a 24-amino acid polypeptide, has been identified to have multiple neuroprotective functions, the level of humanin in plasma has been demonstrated to decrease with age, which likely limits the effects against stroke injury. A potent humanin analogue, S14G-humanin (HNG), generated by replacement of Ser14 with glycine, has been demonstrated to have 1,000-fold stronger biological activity than humanin. The p...
Source: Experimental and Therapeutic Medicine - October 19, 2017 Category: General Medicine Tags: Exp Ther Med Source Type: research
4-((5-(Tert-butyl)-3-chloro-2-hydroxybenzyl) amino)-2-hydroxybenzoic acid protects against oxygen-glucose deprivation/reperfusion injury
Publication date: 1 July 2018 Source:Life Sciences, Volume 204 Author(s): Yuexinzi Jin, Xuelian Tang, Xiang Cao, Linjie Yu, Jian Chen, Haoran Zhao, Yan Chen, Lijuan Han, Xinyu Bao, Fei Li, Yun Xu Aims Oxidative stress is one of the most important pathological mechanisms which could aggravate ischemic stroke injury. In order to seek for better treatment therapies to alleviate stroke injury, novel chemicals have been synthetized. In the present study, a new compound 4-((5-(tert-butyl)-3-chloro-2-hydroxybenzyl) amino)-2- hydroxybenzoic acid, named LX009, was used to determine whether it could reduce the oxidative stress caus...
Source: Life Sciences - May 18, 2018 Category: Biology Source Type: research
Neuroprotective Effects of Isosteviol Sodium through Increasing CYLD by the Downregulation miRNA-181b.
In this study, we found that miR-181b expression was significantly decreased in N2A neuroblastoma cells after CoCl2-induced hypoxic injury in vitro. We further found, via western blot analysis and quantitative polymerase chain reaction assay, that altering miR-181b expression could induce changes in one of its target proteins, cylindromatosis (CYLD). Specifically, upregulation and downregulation of miR-181b (through transfection of either pre- or small interfering miR-181b, respectively) could negatively regulate CYLD protein levels as well as N2A cell survival rate and apoptosis following CoCl2-induced injury. Furthermore...
Source: Brain Research Bulletin - May 25, 2018 Category: Neurology Authors: Zhang H, Zan J, Zhong K, Lu M, Sun X, Tan W Tags: Brain Res Bull Source Type: research
Long non-coding RNA HOXA11-AS regulates ischemic neuronal death by targeting miR-337-3p/YBX1 signaling pathway: protective effect of dexmedetomidine
This study aimed to explore the possible link between Dex and HOXA11-AS in protecting neuronal cells from by ischemia/reperfusion-induced apoptosis. We used oxygen-glucose deprivation and reoxygenation (OGD/R) in mouse neuroblastoma Neuro-2a cells and middle cerebral artery occlusion (MACO) mouse model to test the link. We found that Dex significantly alleviated OGD/R-induced DNA fragmentation, cell viability and apoptosis, and rescued the decreased HOXA11-AS expression after ischemic damage in Neuro-2a cells. Gain-/loss-of-function studies revealed that HOXA11-AS promoted proliferation, inhibited apoptosis in Neuro-2a cel...
Source: Aging - April 14, 2023 Category: Biomedical Science Authors: Fei Yan Pinxiao Wang Xiaojian Yang Fuli Wang Source Type: research
Silibinin exerts neuroprotective effects against cerebral hypoxia/reoxygenation injury by activating the GAS6/Axl pathway
This study aimed to investigate the protective effects of SIL against cerebral ischemia-reperfusion injury in neuroblastoma N2a cells, and the mechanisms involved. Firstly, the toxicity of SIL was evaluated, and safe concentrations were chosen for subsequent experiments. Then, SIL exerts significant neuroprotection against hypoxia/reoxygenation (HR) injury in N2a cells, as manifested by increased cell viability, decreased apoptotic rate, LDH, and ROS generation. Additionally, SIL was found to inhibit HR-induced apoptosis, mitochondria dysfunction, and oxidative stress. However, silencing of GAS6 inhibited the neuroprotecti...
Source: Toxicology - August 6, 2023 Category: Toxicology Authors: Weiping Li Zhe Zhang Jiawen Li Jun Mu Meng Sun Xue Wu Xiaochen Niu Yang Yang Huanle Yan Xiaoling Xu Chengxu Xue Lu Qian Ye Tian Source Type: research
Blockade of Ser16-Hsp20 Phosphorylation Attenuates Neuroprotection Dependent Upon Bcl-2 and Bax.
In conclusion, our data demonstrated that increased Hsp20 and Hsp20 (S16D) expression in mouse N2A neuroblastoma cells protected against ischemia-reperfusion injury, the neuroprotective mechanism may be related to regulate Bcl-2 and Bax expression. However, blockade of Ser16-Hsp20 phosphorylation attenuated the neuroprotective effects of Hsp20. Therefore, Hsp20 and factors that contribute to regulation of phosphorylation on Ser16 of Hsp20 are potential new therapeutic targets for the treatment of cerebral ischemia-reperfusion injury.
PMID: 23713735 [PubMed - as supplied by publisher]
Source: Current Neurovascular Research - May 24, 2013 Category: Neurology Authors: Zeng L, Tan J, Lu W, Hu Z Tags: Curr Neurovasc Res Source Type: research
Neuroprotective activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in rodent models of brain ischemia
In conclusion, the present study indicates that 4R has a protective effect in rodent ischemic stroke models. Inhibition of ICAM-1 expression and restoration of Akt phosphorylation are the possible mechanisms involved in cellular protection by 4R.
Source: Neuroscience - March 5, 2015 Category: Neuroscience Source Type: research
Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis.
This study was aimed to investigate whether knockdown of Id2 in neuronal cells could protect them from hypoxic and ischemic injury both in vitro and in vivo. Flow cytometric analysis was employed to assess neuronal apoptosis in CoCl2-treated neuroblastoma B35 cells engineered to overexpress or knockdown Id2 expression. In vivo knockdown of Id2 was performed in Sprague-Dawley rats by a single intracerebroventricular injection of Cy3-labeled and cholesterol-modified Id2-siRNA. We found that knockdown of Id2 attenuated H/I-induced neuronal apoptosis in vitro while overexpression of Id2 produced an opposite effect. In a rat mo...
Source: Behavioural Brain Research - July 14, 2015 Category: Neurology Authors: Guo L, Yang X, Lin X, Lin Y, Shen L, Nie Q, Ren L, Guo Q, Que S, Qiu Y Tags: Behav Brain Res Source Type: research
