scholarly journals Oxidative stress regulates the ubiquitin–proteasome system and immunoproteasome functioning in a mouse model of X-adrenoleukodystrophy

Brain ◽  
2013 ◽  
Vol 136 (3) ◽  
pp. 891-904 ◽  
Author(s):  
Nathalie Launay ◽  
Montserrat Ruiz ◽  
Stéphane Fourcade ◽  
Agatha Schlüter ◽  
Cristina Guilera ◽  
...  
2006 ◽  
Vol 2006 (Spring) ◽  
Author(s):  
Silke Meiners ◽  
Andrea Weller ◽  
Antje Ludwig ◽  
Karl Stangl ◽  
Verena Stangl

2005 ◽  
Vol 19 (14) ◽  
pp. 2051-2053 ◽  
Author(s):  
Asangi R. K. Kumarapeli ◽  
Kathleen M. Horak ◽  
Joseph W. Glasford ◽  
Jie Li ◽  
Quanhai Chen ◽  
...  

2015 ◽  
Vol 402 (1-2) ◽  
pp. 193-202 ◽  
Author(s):  
Luiz Henrique Soares de Andrade ◽  
Wilson Max Almeida Monteiro de Moraes ◽  
Eduardo Hiroshi Matsuo Junior ◽  
Elizabeth de Orleans Carvalho de Moura ◽  
Hanna Karen Moreira Antunes ◽  
...  

2021 ◽  
Author(s):  
Saba Ubaid ◽  
Shivani Pandey ◽  
Mohd. Sohail Akhtar ◽  
Mohammad Rumman ◽  
Babita Singh ◽  
...  

Abstract Camel milk is rich in nutritional factors, such as α- Lactalbumin, and important for brain development. It is known to act as a potential therapeutic candidate for brain disorder via regulation of inflammatory and apoptotic pathways. Mechanisms that are critically involved with Parkinson’s disease (PD) are apoptosis, inflammation, and oxidative stress, and the aberrated ubiquitin-proteasome system. Adverse effects of current therapies are imposing the need for the development of natural neuroprotective agents that are very effective and have fewer or no side effects. The present study aimed to evaluate the potential activity of camel α-Lactalbumin (α-LA) in rotenone induced in-vitro PD model. In this study, we hypothesized the use of camel α-lactalbumin as an effective curative agent for PD. The mechanism of action of camel α-lactalbumin was investigated by assessing the effect of α-LA on the level of nitric oxide, NADH, MMP9, inflammatory markers, and on the expression level of SIRT1 and FOXO3a in SH-SY5Y cell line. Overall, the results revealed the potent neuroprotective efficacy of α-Lactalbumin in rotenone-induced PD model via effectively modulating apoptotic pathways, oxidative stress, and neuroinflammatory cascades. Conclusively, these findings confirmed that α-LA could be a biologically effective protective agent against rotenone induced neurotoxic impacts and neurobehavioral aberrations.


Cell Cycle ◽  
2011 ◽  
Vol 10 (8) ◽  
pp. 1200-1207 ◽  
Author(s):  
Annett Koch ◽  
Janos Steffen ◽  
Elke Krüger

2003 ◽  
Vol 21 (8) ◽  
pp. 897-902 ◽  
Author(s):  
Kristina Lindsten ◽  
Victoria Menéndez-Benito ◽  
Maria G Masucci ◽  
Nico P Dantuma

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