Tauroursodeoxycholic acid inhibits the cytosolic Ca ++ increase in human neutrophils stimulated by formyl-methionyl-leucyl-phenylalanine
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 171, Issue: 3, Page: 1115-1121
1990
- 18Citations
- 1Captures
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Metrics Details
- Citations18
- Citation Indexes18
- 18
- CrossRef14
- Captures1
- Readers1
Article Description
The effect of the cytoprotective bile acid tauroursodeoxycholic acid (TUDCA) on basal cytosolic free Ca ++ (Ca ++ ) i and receptor-mediated (Ca ++ ) i increase was studied in human polymorphonuclear neutrophils using the fluorescent dye quin2. Basal levels of (Ca ++ ) i were 96 ± 6 nmol/1 (mean ± SEM, n=48). TUDCA and its cytotoxic epimer taurochenodeoxycholic acid (TCDCA) at 500 μmol/l increased (Ca ++ ) i by 31 ± 12 and 27 ± 7 nmol/l, respectively (n=6, p<0.05). Stimulation of neutrophils with the chemotactic tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP; 10 −7 mol/l) induced a (Ca ++ ) i increase of 200 ± 32 nmol/l which was inhibited after preincubation with TUDCA (500 μmol/l) or TUDCA-TCDCA (500 μmol/l, each) by 60.1% and 59.5%, respectively, but not with TCDCA (500 μmol/l) alone. The inhibitory effect of TUDCA on FMLP-induced (Ca ++ ) i increase was strongly concentration-dependent and was nearly complete at 1000 μmol/l. Since (Ca ++ ) i is discussed as a mediator of cellular injury we hypothesize that TUDCA may exert its protective effects at least partly via inhibition of (Ca ++ ) i -mediated cytotoxic processes.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0006291X90908003; http://dx.doi.org/10.1016/0006-291x(90)90800-3; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0025078256&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/2222431; http://linkinghub.elsevier.com/retrieve/pii/0006291X90908003; http://api.elsevier.com/content/article/PII:0006291X90908003?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:0006291X90908003?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/0006291X90908003; http://dx.doi.org/10.1016/0006-291x%2890%2990800-3; https://dx.doi.org/10.1016/0006-291x%2890%2990800-3
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