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Expression of cyclooxygenase enzymes in rat hypothalamo-pituitary-adrenal axis - Effects of endotoxin and glucocorticoids
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UNSPECIFIED (2001) Expression of cyclooxygenase enzymes in rat hypothalamo-pituitary-adrenal axis - Effects of endotoxin and glucocorticoids. ENDOCRINE, 16 (2). pp. 123-131. ISSN 0969-711X.
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Abstract
Prostaglandins play a key role in mediating the hypothalamo-pituitary-adrenocortical (HPA) responses to immune insults. This study aimed to provide some insight into the relative contributions of the constitutive and inducible forms of cyclooxygenase (COX-1 and COX-2) to the generation of these prostanoids by examining the effects of (1) endotoxin treatment on the expression of COX-1 and COX-2 mRNAs in the various components of the HPA axis in control and glucocorticoid pretreated rats, and (2) selective inhibition of COX-2 on the production of corticosterone by adrenal tissue in vitro. Endotoxin caused a marked rise in COX-2 mRNA in the adrenal gland that was evident 3 and 6 h after the injection and was prevented by pretreatment with dexamethasone. It also induced a modest increase in COX-2 mRNA in the hypothalamus but not in the hippocampus or anterior pituitary gland. By contrast, COX-1 mRNA was largely unaffected by the drug treatments in all tissues studied. In vitro the selective COX-2 inhibitor SC-236 caused a marked reduction in adrenocorticotropic hormone-driven corticosterone release, as did the nonselective COX inhibitor, indomethacin. These results support a role of COX-2 in the manifestation of the HPA responses to endotoxin, particularly within the adrenal gland.
Item Type: | Journal Article | ||||
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Subjects: | R Medicine > RC Internal medicine | ||||
Journal or Publication Title: | ENDOCRINE | ||||
Publisher: | HUMANA PRESS INC | ||||
ISSN: | 0969-711X | ||||
Official Date: | November 2001 | ||||
Dates: |
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Volume: | 16 | ||||
Number: | 2 | ||||
Number of Pages: | 9 | ||||
Page Range: | pp. 123-131 | ||||
Publication Status: | Published |
Data sourced from Thomson Reuters' Web of Knowledge
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