Role of oxidative stress and inflammation in hypoxia-induced cerebral edema: a molecular approach

Role of oxidative stress and inflammation in hypoxia-induced cerebral edema: a molecular approach

The present study reports the possible role of oxidative stress and inflammation (role of nuclear factor, NFkB) in hypoxia-induced transvascular leakage in brain of rats. The rats were exposed to a simulated altitude of 25,000 ft for different durations: 0, 3, 6, 12, 24, and 48h. Brain water content...

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Bibliographic Details
Published in:High altitude medicine & biology Vol. 11; no. 3; p. 231
Main Authors: Himadri, P, Kumari, Sarada S, Chitharanjan, M, Dhananjay, S
Format: Journal Article
Language:English
Published: United States 01-10-2010
Subjects:
Analysis of Variance
Animals
Brain Edema - metabolism
Brain Edema - physiopathology
Cell Adhesion Molecules - metabolism
Cytokines - metabolism
DNA - metabolism
Environmental Exposure - adverse effects
Hypoxia, Brain - metabolism
Hypoxia, Brain - physiopathology
Inflammation - metabolism
Inflammation - physiopathology
Male
NF-kappa B - metabolism
Oxidative Stress
Physical Conditioning, Animal
Random Allocation
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species - metabolism
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Summary:The present study reports the possible role of oxidative stress and inflammation (role of nuclear factor, NFkB) in hypoxia-induced transvascular leakage in brain of rats. The rats were exposed to a simulated altitude of 25,000 ft for different durations: 0, 3, 6, 12, 24, and 48h. Brain water content, transvascular leakage, oxidative stress, and proinflammatory parameters were studied at different durations of hypoxic exposure. The results revealed that maximum increase in transvascular leakage in brain of rats was observed at 24h of hypoxic exposure (240.16 ± 1.95 relative fluorescence units (r.f.u)/g tissue) compared with control (100.58 ± 1.79 r.f.u/g tissue). There was a significant increase in reactive oxygen species (ROS) and lipid peroxidation (MDA), with concomitant reduction in antioxidants. Hypoxic exposure resulted in a significant increase in NFκB protein expression levels and in the DNA binding activity in the 24-h hypoxic exposure (p<0.001) compared with control. There was a significant increase in proinflammatory cytokines, with concomitant upregulation of cell adhesion molecules. Simultaneously, to rule out the fact that inflammation causes cerebral edema, the rats were pretreated with curcumin (100 mg/kg body weight) 1h prior to 24-h hypoxia. Curcumin pretreatment significantly attenuated the hypoxia-induced cerebral transvascular leakage (p<0.05), with concomitant downregulation in the expression of brain NFκB levels (p<0.001). The present study therefore reveals that inflammation (NFκB) plays a significant role in hypoxia-induced cerebral edema.
ISSN:1557-8682
DOI:10.1089/ham.2009.1057