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Condition: Mitochondrial Disease
Cancer: Neuroblastoma

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Total 19 results found since Jan 2013.

11,12-Diacetyl-carnosol Protects SH-SY5Y Cells from Hydrogen Peroxide Damage through the Nrf2/HO-1 Pathway
CONCLUSION: These results demonstrate that NO.20 protects SH-SY5Y cells from H2O2-induced neurotoxicity by activating the Nrf2/HO-1 pathway. Thus, the neuroprotective and antioxidative stress effects of NO.20 may make it a promising neuroprotective compound for AD treatment.PMID:35620405 | PMC:PMC9129961 | DOI:10.1155/2022/4376812
Source: Evidence-based Complementary and Alternative Medicine - May 27, 2022 Category: Complementary Medicine Authors: Qingyi Luo Weiyan Hu Haofei Yu Rongping Zhang Xinglong Chen Source Type: research

Beneficial effects of PGC-1 α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity.
CONCLUSIONS: Our results indicated that PGC-1α rescues the effects of MPTP-induced mitochondrial dysfunction in C57BL mice. PMID: 31634150 [PubMed - as supplied by publisher]
Source: Aging - October 20, 2019 Category: Biomedical Science Authors: Wang Y, Chen C, Huang W, Huang M, Wang J, Chen X, Ye Q Tags: Aging (Albany NY) Source Type: research

Eclalbasaponin I causes mitophagy to repress oxidative stress-induced apoptosis via activation of p38 and ERK in SH-SY5Y cells.
In this study, pretreatment with EcI in SH-SY5Y cells significantly activated the p38-mitogenactivated protein kinase (p38), the extracellular regulated protein kinase (ERK), whereas it did not affect the c-jun NH2 terminal kinases (JNK). In accordance with the initial findings, EcI-induced neuroprotective effect was attenuated by SB203580 (SB, a p38 inhibitor) or FR180204 (FR, an ERK inhibitor), being further confirmed by specific small interfering RNA (siRNA). Inhibition of either p38 or ERK up-regulated the apoptosis induction in EcI- and H2O2-cotreated cells. Furthermore, p38 or ERK suppression enhanced intracellular a...
Source: Free Radical Research - June 14, 2019 Category: Research Tags: Free Radic Res Source Type: research

Detailed Dissection of UBE3A-Mediated DDI1 Ubiquitination
Discussion Poly-ubiquitinated proteins targeted for degradation might be recognized directly by proteasomal receptors or by proteasomal shuttling proteins. The first shuttling proteins – Ddi1, Rad23 and Dsk2 – were identified and characterized in Saccharomyces cerevisiae (Lambertson et al., 1999; Kaplun et al., 2005). Proteasomal shuttles contain an N-terminal ubiquitin-like (UBL) domain that interacts with the 26S proteasome (Finley, 2009), and a C-terminal ubiquitin-binding domain domain (UBD) that binds to ubiquitin or poly-ubiquitin chains (Bertolaet et al., 2001). When ubiquitinated, substrates are capt...
Source: Frontiers in Physiology - May 2, 2019 Category: Physiology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Inhibition of the Nrf2/HO-1 Axis Suppresses the Mitochondria-Related Protection Promoted by Gastrodin in Human Neuroblastoma Cells Exposed to Paraquat
AbstractMitochondria are double-membrane organelles involved in the transduction of energy from different metabolic substrates into adenosine triphosphate (ATP) in mammalian cells. The oxidative phosphorylation system is comprised by the activity of the respiratory chain and the complex V (ATP synthase/ATPase). This system is dependent on oxygen gas (O2) in order to maintain a flux of electrons in the respiratory chain, since O2 is the final acceptor of these electrons. Electron leakage from this complex system leads to the continuous generation of reactive species in the cells. The mammalian cells exhibit certain mechanis...
Source: Molecular Neurobiology - July 11, 2018 Category: Neurology Source Type: research

Pinocembrin Suppresses H 2 O 2 -Induced Mitochondrial Dysfunction by a Mechanism Dependent on the Nrf2/HO-1 Axis in SH-SY5Y Cells
AbstractMitochondria are susceptible to redox impairment, which has been associated with neurodegeneration. These organelles are both a source and target of reactive species. In that context, there is increasing interest in finding natural compounds that modulate mitochondrial function and mitochondria-related signaling in order to prevent or to treat diseases involving mitochondrial impairment. Herein, we investigated whether and how pinocembrin (PB) would prevent mitochondrial dysfunction elicited by the exposure of human neuroblastoma SH-SY5Y cells to hydrogen peroxide (H2O2). PB (25  μM) was administrated for 4 h be...
Source: Molecular Neurobiology - January 12, 2017 Category: Neurology Source Type: research

Pterostilbene attenuates high glucose-induced oxidative injury in hippocampal neuronal cells by activating nuclear factor erythroid 2-related factor 2
Publication date: Available online 9 January 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Author(s): Yang Yang, Chongxi Fan, Bodong Wang, Zhiqiang Ma, Dongjin Wang, Bing Gong, Shouyin Di, Shuai Jiang, Yue Li, Tian Li, Zhi Yang, Erping Luo In the present study, neuroblastoma (SH-SY5Y) cells were used to investigate the mechanisms mediating the potential protective effects of pterostilbene (PTE) against mitochondrial metabolic impairment and oxidative stress induced by hyperglycemia for mimicking the diabetic encephalopathy. High glucose medium (100 mM) decreased cellular viability after 24 h...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - January 8, 2017 Category: Molecular Biology Source Type: research

Protection from interferon ‐β‐induced neuronal apoptosis through stimulation of muscarinic acetylcholine receptors coupled to ERK1/2 activation
Conclusions and implicationsStimulation of mAChRs counteracted IFN‐β‐induced neuronal apoptosis through the activation of ERK1/2 signalling. The data indicate that activation of ERK1/2‐coupled mAChRs may be an effective strategy for preventing IFNs neurotoxicity. This article is protected by copyright. All rights reserved.
Source: British Journal of Pharmacology - July 30, 2016 Category: Drugs & Pharmacology Authors: Maria C. Olianas, Simona Dedoni, Pierluigi Onali Tags: RESEARCH PAPER Source Type: research

NICOTINAMIDE N-METHYLTRANSFERASE increases complex I activity IN SH-SY5Y cells via SIRTUIN-3.
Abstract Nicotinamide N-methyltransferase (NNMT, E.C. 2.1.1.1) N-methylates nicotinamide to 1-methylnicotinamide. We have previously shown that NNMT is significantly overexpressed in the brains of patients who have died of Parkinson's disease, and others have shown that NNMT is significantly overexpressed in a variety of diseases ranging from cancer to hepatic cirrhosis. In vitro overexpression has revealed many cytoprotective effects of NNMT, in particular increased complex I activity and ATP synthesis. Although this appears to be mediated by an increase in 1-methylnicotinamide production, the molecular mechanism...
Source: Biochemical and Biophysical Research communications - October 8, 2015 Category: Biochemistry Authors: Liu KY, Mistry RJ, Aguirre CA, Fasouli ES, Thomas MG, Klamt F, Ramsden DB, Parsons RB Tags: Biochem Biophys Res Commun Source Type: research

Elevation of Sestrin-2 expression attenuates Sevoflurane induced neurotoxicity
In this study, our results indicated that administration of Sevoflurane elevated the gene and protein expression of Sestrin-2 in a dose dependent manner in human neuroblastoma M17 cells. It was shown that silence of Sestrin-2 by small RNA interference (siRNA) ominously exacerbated the increase in intracellular ROS and reduction of SOD activity induced by Sevoflurane treatment. Notably, knockdown of Sestrin-2 in M17 cells significantly increases the number of apoptotic cells after treatment with Sevoflurane. Mechanistically, we also found that Sevoflurane treatment resulted in a reduced amount of the cytosolic anti-apoptoti...
Source: Metabolic Brain Disease - September 5, 2015 Category: Neurology Source Type: research