TUESDAY, Dec. 25 (HealthDay News) -- Stress mediators regulate inflammatory pathways in the rat brain cortex in response to acute restraint stress, according to research published online Dec. 13 in Endocrinology.
Borja Garcia-Bueno, and colleagues from University Complutense in Madrid, Spain, examined the role of the stress mediators catecholamines, glucocorticoids and glutamate in the stress-related effects -- prostaglandin synthesis, cyclooxygenase-2 (COX-2) regulation, peroxisome proliferator-activated receptor gamma (PPAR-γ) activation -- of acute restraint stress in rats.
The researchers found that inhibiting catecholamines in the central nervous system reduced COX-2 overexpression, thereby regulating prostaglandin synthesis, and reduced PPAR-γ activation. Stress-induced glucocorticoids affected prostaglandin synthesis by interacting with mineralocorticoid and glucocorticoid receptors. Blocking one type of glucocorticoid receptor downregulated COX-2, thereby negatively regulating prostaglandin synthesis, and reduced PPAR-γ activity and expression.
"In conclusion, we show here that the main stress mediators: catecholamines, glucocorticoids and glutamate, concomitantly regulate the activation of proinflammatory and anti-inflammatory pathways in a possible co-regulatory mechanism of the inflammatory process induced in rat brain cortex by acute restraint stress exposure," the authors write.
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