Evidence that carbon monoxide stimulates prostaglandin endoperoxide synthase activity in rat hypothalamic explants and in primary cultures of rat hypothalamic astrocytes.

摘要: Carbon monoxide (CO) shares with nitric oxide (NO) the ability to modulate release of hypophysiotropic peptides from rat hypothalamic explants. While both gases are believed act as neural messengers in brain via activation soluble guanylyl cyclase, latter is almost undetectable hypothalamus. NO has been shown exert some its biological actions through modulation prostaglandin endoperoxide synthase (PGHS) activity. We have, therefore, investigated whether CO also can use PGHS a signaling pathway Endogenous produced equimolar amounts biliverdin (BV) by catabolism hemin heme oxygenase (HO). Hemin, two inhibitors HO, zinc-protoporphyrin-9 (ZnPP9) and tin-mesoporphyrin-9 (SnMP9), ferrous hemoglobin (Hb), indomethacin dexamethasone (DEX) were used pharmacological tools. Prostaglandin E2 (PGE2) released explants or primary cultures astrocytes was taken marker It found that: (1) evokes an increase PGE2 explants; (2) this effect counteracted ZnPP9, SnMP9, Hb indomethacin; (3) metallo-porphyrins indomethacin, but not Hb, able inhibit basal (4) does inhibit, even potentiates, stimulatory on astrocytes. The evidence presented here suggests that endogenous exogenously added associated production This be attributed formation CO, since other end-product BV, enhance release. Thus, at least effects level might mediated pathway.