ArticleJapanese journal of ophthalmology2009
Antiglaucoma drug GLC756 and its effect on cellular cAMP and tumor necrosis factor alpha release in vitro of activated human monocytic leukemia cells.
Article in Japanese journal of ophthalmology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeGLC756, a putative antiglaucoma drug with dopamine D(2) agonist and D(1) antagonist properties, significantly decreases tumor necrosis factor alpha (TNF-alpha) levels in lipopolysaccharide (LPS)-induced rats. The present study describes the effects of GLC756 on cellular adenosine 3', 5'-cyclic monophosphate (cAMP) in relation to TNF-alpha production on LPS-stimulated human acute monocytic leukemia cells.
methodsA human peripheral blood acute monocytic leukemia cell line (THP-1) was activated via LPS. THP-1 cells were incubated with GLC756 or betamethasone (positive control) at concentrations of 1, 10, and 30 microM. The TNF-alpha concentration in supernatant and cAMP levels in cellular extract were measured by enzyme-linked immunosorbent assay 0,1, 2.5, 4.5, 7, and 24 h post-activation.
resultsCompared with LPS controls, both GLC756 at 30 muM and betamethasone at > or =1 microM had a significant inhibitory effect on TNF-alpha release from THP-1 cells 2.5 to 24 h post-activation. Parallel to the TNF-alpha decrease, GLC756 induced significant increases of cellular cAMP 2.5 and 7 h post-activation. Betamethasone had no effect on the cellular cAMP level.
conclusionIntracellular signaling pathway leading to inhibition of the production of the proinflammatory cytokine TNF-alpha after GLC756 treatment might be mediated through the second messenger cAMP.
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