Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Rat hypothalamic corticotropin-releasing hormone secretion in vitro is stimulated by interleukin-1 in an eicosanoid-dependent manner. 212 10

Anterior pituitary quarters were incubated in vitro and the release of beta-endorphin-like (beta-End-IR) and adrenocorticotropin-like immunoreactivity (ACTH-IR) was determined. The effect of phospholipase A2 as well as the effect of various compounds known to influence arachidonic acid metabolism under certain conditions were examined. Phospholipase A2 increased the release of beta-End-IR and ACTH-IR. This effect was reversible, concentration-dependent (1-400 ng/ml) and inhibited in calcium-free medium and in the presence of CoCl2 (5 mM) or phospholipase A2 inhibitors (p-bromophenacylbromide, 21 microM; mepacrine, 1 mM). The phospholipase A2-induced beta-End-IR release was accompanied by the release of prostaglandin E2. Inhibition of cyclooxygenase activity by indomethacin (14 or 140 microM) did not change beta-End-IR release induced by phospholipase A2 (5 ng/ml). The effects of blockers of lipoxygenase (nordihydroguaiaretic acid, NDGA; AA861) or lipoxygenase plus cyclooxygenase (BW755C; eicosatetraynoic acid, ETYA) on phospholipase A2-induced release of beta-End-IR were diverse. BW755C (up to 250 microM) and AA861 (up to 100 microM) produced no effect. However, NDGA or ETYA inhibited phospholipase A2-induced beta-End-IR release. NDGA (100 microM) produced a maximum inhibition by about 40% (p less than 0.05), whereas ETYA (100 microM) produced a maximum inhibition by about 85% (p less than 0.001). These data are consistent with the view that phospholipase A2 releases endogenous arachidonic acid which is transformed into products which stimulate ACTH and beta-endorphin release from the corticotrophs; the metabolizing enzyme (possibly a lipoxygenase or epoxygenase) is sensitive to NDGA and especially to ETYA.
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PMID:Effect of various blockers of arachidonic acid metabolism on release of beta-endorphin- and adrenocorticotropin-like immunoreactivity induced by phospholipase A2 from rat adenohypophysis in vitro. 301 92

This study was performed to examine an involvement of adenohypophysial arachidonic acid metabolites in the local mechanisms controlling the release of peptide hormones from the corticotrope cells of the anterior pituitary gland. Therefore, we investigated the effect of blockers of the lipoxygenase (nordihydroguaiaretic acid, NDGA), cyclooxygenase (indomethacin) or both of these enzyme systems (BW755C; eicosatetraynoic acid, ETYA) on the release of beta-endorphin-like (beta-E-IR) and adrenocorticotropin-like immunoreactivity (ACTH-IR) from rat anterior pituitary quarters incubated in vitro. NDGA and ETYA did not influence the basal release of beta-E- and ACTH-IR. However, upon stimulation by arginine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor (CRF(1-41], NDGA inhibited beta-E-IR release by 40%. ETYA inhibited AVP-induced release of beta-E- and ACTH-IR by 75%. Indomethacin and BW755C (lower concentration) enhanced beta-E-IR release, induced by AVP, by about 100%, whereas BW755C (higher concentration) had no effect. When indomethacin was present, NDGA, ETYA and BW755C (higher concentration) inhibited AVP-induced release of beta-E- and ACTH-IR. Prostaglandin E2 (PGE2) inhibited beta-E-IR release in response to AVP but failed to do so in the presence of NDGA. 12-OH-5,8,10,14-eicosatetraenoic acid (12-HETE) had no effect. When anterior pituitary quarters were incubated with 3H-arachidonic acid (3H-AA), NDGA and BW755C (higher concentration) but not indomethacin and BW755C (lower concentration) blocked the formation of a metabolite which co-migrated with 12-HETE on thin-layer chromatography.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin and adrenocorticotropin release from rat adenohypophysis in vitro: evidence for local modulation by arachidonic acid metabolites of the cyclooxygenase and lipoxygenase pathway. 609 88