TY - JOUR
T1 - Kinetics of the neuroinflammation-oxidative stress correlation in rat brain following the injection of fibrillar amyloid-β onto the hippocampus in vivo
AU - Rosales-Corral, Sergio
AU - Tan, Dun-xian
AU - Reiter, Russel J.
AU - Valdivia-Velázquez, Miguel
AU - Acosta-Martínez, J. Pablo
AU - Ortiz, Genaro G.
N1 - Funding Information:
This work was supported by the Consejo Nacional de Ciencia y Tecnologı́a [CONACYT], México, and the Instituto Mexicano del Seguro Social [IMSS].
PY - 2004/5
Y1 - 2004/5
N2 - The purpose of this study was to describe - following the injection of a single intracerebral dose of fibrillar amyloid-β1-40 in vivo - some correlations between proinflammatory cytokines and oxidative stress indicators in function of time, as well as how these variables fit in a regression model. We found a positive, significant correlation between interleukin (IL)-1β or IL-6 and the activity of the glutathione peroxidase enzyme (GSH-Px), but IL-1β or IL-6 maintained a strong, negative correlation with the lipid peroxidation (LPO). The first 12 h marked a positive correlation between IL-6 and tumor necrosis factor-alpha (TNF-α), but starting from the 36 h, this relationship became negative. We found also particular patterns of behavior through the time for IL-1β, nitrites and IL-6, with parallel or sequential interrelationships. Results shows clearly that, in vivo, the fibrillar amyloid-β (Aβ) disrupts the oxidative balance and initiate a proinflammatory response, which in turn feeds the oxidative imbalance in a coordinated, sequential way. This work contributes to our understanding of the positive feedbacks, focusing the "cytokine cycle" along with the oxidative stress mediators in a complex, multicellular, and interactive environment.
AB - The purpose of this study was to describe - following the injection of a single intracerebral dose of fibrillar amyloid-β1-40 in vivo - some correlations between proinflammatory cytokines and oxidative stress indicators in function of time, as well as how these variables fit in a regression model. We found a positive, significant correlation between interleukin (IL)-1β or IL-6 and the activity of the glutathione peroxidase enzyme (GSH-Px), but IL-1β or IL-6 maintained a strong, negative correlation with the lipid peroxidation (LPO). The first 12 h marked a positive correlation between IL-6 and tumor necrosis factor-alpha (TNF-α), but starting from the 36 h, this relationship became negative. We found also particular patterns of behavior through the time for IL-1β, nitrites and IL-6, with parallel or sequential interrelationships. Results shows clearly that, in vivo, the fibrillar amyloid-β (Aβ) disrupts the oxidative balance and initiate a proinflammatory response, which in turn feeds the oxidative imbalance in a coordinated, sequential way. This work contributes to our understanding of the positive feedbacks, focusing the "cytokine cycle" along with the oxidative stress mediators in a complex, multicellular, and interactive environment.
KW - Amyloid-β
KW - Cytokine
KW - Interleukin
KW - Kinetics
KW - Neuroinflammatory response
KW - Oxidative stress
KW - Tumor necrosis factor
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U2 - 10.1016/j.jneuroim.2004.01.005
DO - 10.1016/j.jneuroim.2004.01.005
M3 - Article
C2 - 15081245
AN - SCOPUS:1842738222
SN - 0165-5728
VL - 150
SP - 20
EP - 28
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -