Detail of "11028-71-0"

Reference

Hydrocortisone selectively inhibits IgE-dependent arachidonic acid release from rat peritoneal mast cells

Hydrocortisone selectively inhibits IgE-dependent arachidonic acid release from rat peritoneal mast cells. Heiman, Ann S.; Crews, Fulton T. (Coll. Med., Univ. Florida, Gainesville, FL 32610, USA). Prostaglandins, 27(2), 335-43 (English) 1984. CODEN: PRGLBA. ISSN: 0090-6980. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 15 Purified rat mast cells were used to study the effects of anti-inflammatory steroids (hydrocortisone [50-23-7]) on the release of 1-14C-labeled arachidonic acid (AA) [506-32-1] and metabolites. Release of [1-14C]AA and metabolites by concanavalin A [11028-71-0], the antigen ovalbumin, and anti-IgE antibody was markedly reduced by glucocorticoid treatment. Neither the total incorporation of [1-14C]AA nor the distribution into phospholipids was altered by hydrocortisone pretreatment.There are some commonly used reagents with their cas registry numbers 50-00-0 and 41598-07-6 in this article. Glucocorticoid pretreatment did not alter [1-14C]AA release stimulated by somatostatin [51110-01-1], compd. 48/80, or the Ca ionophore, A 23187. Antiinflammatory steroids apparently selectively inhibit Ig-dependent release of arachidonic acid from rat mast cells. These findings question the role of lipomodulin and macrocortin as general phospholipase inhibitors and suggest that they may be restricted to Ig stimuli. .

In vitro inhibition of histamine release from mouse mast cells and human basophils by an anthranilic acid derivative

In vitro inhibition of histamine release from mouse mast cells and human basophils by an anthranilic acid derivative. Zampini, P.; Riviera, A.In this study， 52665-69-7 and 53902-12-8 are also used. P.; Tridente, G. (Univ. Verona, Verona 37100, Italy). Int. J. Immunopharmacol., 5(5), 431-5 (English) 1983. CODEN: IJIMDS. ISSN: 0192-0561. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Optimal conditions for in vitro histamine [51-45-6] release mediated either by Con A [11028-71-0] (3 mg/mL) or by ionophore A23187 [52665-69-7] (1 mg/mL) were established for mouse peritoneal mast cells and human normal basophils. In both systems N-(3',4'-dimethoxycinnamoyl)anthranilic acid (I) [53902-12-8] exerts potent inhibiting effects on histamine release after short term (1-5 min) in vitro preincubation. At concns. of 1 mM for mouse mast cells and 3 mM for normal human basophils, I inhibits up to 95% Con A-induced histamine release and >50% ionophore-induced histamine release. Such in vitro effects are more potent than di-Na cromoglycate-mediated inhibition, under similar exptl. conditions, and are resistant to challenge with exceeding doses of the two releasing agents, particularly in the Con A system. Basophils with apparent normal morphol., from a chronic myeloid leukemic patient, were resistant to both challenges. .