Rat hypothalamic corticotropin-releasing hormone secretion is stimulated by interleukin-1 in an eicosanoid-dependent manner

Autor: Bernardini, Renato, Calogero, Aldo Eugenio, Luger, A, Gold, Pw, Chrousos, Gp
Rok vydání: 1990
Předmět:
Male
endocrine system
medicine.medical_specialty
Corticotropin-Releasing Hormone/secretion
Corticotropin-Releasing Hormone
Arachidonic Acids/metabolism
Hypothalamus/drug effects
Indomethacin
Hypothalamus
Arachidonic Acids
Peptide hormone
Biology
Dinoprost
Dexamethasone
Dinoprostone
General Biochemistry
Genetics and Molecular Biology

chemistry.chemical_compound
Internal medicine
medicine
Animals
Masoprocol
Cyclooxygenase Inhibitors
Secretion
Lipoxygenase Inhibitors
General Pharmacology
Toxicology and Pharmaceutics

Arachidonic Acid
Rats
Inbred Strains

General Medicine
5
8
11
14-Eicosatetraynoic Acid

Lipooxygenase Inhibitor
Rats
Nordihydroguaiaretic acid
Endocrinology
chemistry
Eicosanoid
biology.protein
Eicosanoids
Corticotropin-releasing hormone secretion
Arachidonic acid
Cyclooxygenase
hormones
hormone substitutes
and hormone antagonists

Interleukin-1
Zdroj: Life Sciences. 47:1601-1607
ISSN: 0024-3205
DOI: 10.1016/0024-3205(90)90190-3
Popis: We studied the effect of interleukin-1 alpha (IL-1) on corticotropin-releasing hormone (CRH) secretion by explanted rat hypothalami in vitro. We also assessed possible mediation of arachidonic acid metabolites on IL-1-stimulated CRH secretion, by preincubating hypothalami with the cyclooxygenase inhibitor indomethacin (INDO, 1 microM), the lipoxygenase and cyclooxygenase inhibitor eicosatetraynoic acid (ETYA, 10 microM), or the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA, up to 30 microM). In additional experiments, prostaglandins (PG) E2 and F2 alpha were added to the cultures treated with INDO or ETYA. Finally, we investigated the effect of dexamethasone (DEX) on IL-1-stimulated CRH secretion. IL-1 stimulated immunoreactive CRH (iCRH) secretion by explanted hypothalami in a concentration-dependent fashion. Both INDO and ETYA inhibited IL-1-(10nM)-stimulated iCRH secretion, whereas NDGA did not have any effect. The addition of PGF2 alpha (10 nM) restored the secretion of iCRH inhibited by INDO. DEX treatment significantly inhibited IL-1-stimulated iCRH release. Our results suggest that the stimulatory effect of IL-1 on the hypothalamic CRH neuron is mediated by the cyclooxygenase metabolites of arachidonic acid, and, among others, by PGF2 alpha.
Databáze: OpenAIRE