ArticleEndocrine2001
Expression of cyclooxygenase enzymes in rat hypothalamo-pituitary-adrenal axis: effects of endotoxin and glucocorticoids.
Article in Endocrine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia.Endocrine-related cancer · 2016Article
- Repeated predictable stress causes resilience against colitis-induced behavioral changes in mice.Frontiers in behavioral neuroscience · 2014Article
- Cerebrovascular cyclooxygenase-1 expression, regulation, and role in hypothalamic-pituitary-adrenal axis activation by inflammatory stimuli.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Anti-inflammatory effects of angiotensin receptor blockers in the brain and the periphery.Cellular and molecular neurobiology · 2009Review
- Angiotensin II AT1 receptor blockade decreases lipopolysaccharide-induced inflammation in the rat adrenal gland.Endocrinology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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