Linked Life Data

1712816

Source:http://linkedlifedata.com/resource/pubmed/id/1712816

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-8-20
pubmed:abstractText
We determined the ability of hydrocortisone to inhibit rat basophilic leukemia cell mediator release induced by anti-IgE and by neutrophil-derived histamine-releasing activity (HRA-N). Serotonin release induced by HRA-N and anti-IgE was inhibited by 78 +/- 5 and 70 +/- 4%, respectively (IC50 7.5 x 10(-7)M) by hydrocortisone (10(-5)M). HRA-N does not cause arachidonic acid metabolism, however, anti-IgE induced the generation of PGD2 and leukotriene (LT)C4, and the generation of both mediators was inhibited by 10(-5)M hydrocortisone (IC50 = 4.8 x 10(-7)M, and 3.6 x 10(-9)M, respectively). Inhibition required at least 5 to 6 h of hydrocortisone exposure and was maximal after 22 h. The observed effects of hydrocortisone could be reproduced by human recombinant lipocortin-I (5 x 10(-7)M). Hydrocortisone, 10(-5)M, was a less potent inhibitor of calcium ionophore A23187-mediated serotonin release and PGD2 and LTC4 generation (inhibition of 20 +/- 2, 17 +/- 10, and 37 +/- 10%, respectively). Inasmuch as A23187-induced stimulation is not dependent on receptor coupling, the enhanced ability of hydrocortisone to inhibit IgE- and HRA-N-mediated events as compared with A23187 suggests that one possible site of action of hydrocortisone may be interruption of receptor-effector signals. In the presence of arachidonic acid, hydrocortisone-treated cells released as much LTB4 and PGD2 as control cells, however, serotonin release and LTC4 generation were inhibited 50 and 55%, respectively. Thus, these data suggest that hydrocortisone has three possible sites of action: 1) inhibition of phospholipase A2 activity, 2) inhibition of glutathione-s-transferase, and 3) inhibition of serotonin release by a third mechanism, possibly by interrupting the coupling of receptor and effector systems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
667-73
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1712816-Animals, pubmed-meshheading:1712816-Annexins, pubmed-meshheading:1712816-Arachidonic Acid, pubmed-meshheading:1712816-Arachidonic Acids, pubmed-meshheading:1712816-Calcium-Binding Proteins, pubmed-meshheading:1712816-Cytokines, pubmed-meshheading:1712816-Dose-Response Relationship, Drug, pubmed-meshheading:1712816-Histamine Release, pubmed-meshheading:1712816-Humans, pubmed-meshheading:1712816-Hydrocortisone, pubmed-meshheading:1712816-Immunoglobulin E, pubmed-meshheading:1712816-Leukemia, Basophilic, Acute, pubmed-meshheading:1712816-Mast Cells, pubmed-meshheading:1712816-Neutrophils, pubmed-meshheading:1712816-Prostaglandin D2, pubmed-meshheading:1712816-Rats, pubmed-meshheading:1712816-SRS-A, pubmed-meshheading:1712816-Serotonin, pubmed-meshheading:1712816-Tumor Cells, Cultured
pubmed:year
1991
pubmed:articleTitle
Hydrocortisone inhibits rat basophilic leukemia cell mediator release induced by neutrophil-derived histamine releasing activity as well as by anti-IgE.
pubmed:affiliation
National Institutes of Health, National Institute of Allergy and Infectious Diseases, Allergic Diseases Section, Bethesda, MD 20892.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't