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Cyclosporin A inhibits H 2 O 2 ‐induced apoptosis of human fibroblasts
Author(s) -
Sugano Naoyuki,
Ito Koichi,
Murai Seidai
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00312-9
Subject(s) - apoptosis , reactive oxygen species , chemistry , caspase 3 , caspase , pharmacology , cancer research , microbiology and biotechnology , biology , medicine , programmed cell death , biochemistry
Several clinical studies have shown that cyclosporin A (CsA) is effective for treating a variety of chronic inflammatory and autoimmune diseases. Because reactive oxygen species are believed to play a key role in the development of these diseases, causing cell apoptosis, we investigated whether CsA inhibits H 2 O 2 ‐induced apoptosis. Preincubation of human fibroblasts with CsA dose‐dependently decreased H 2 O 2 ‐induced apoptosis. Apoptosis suppression by CsA was correlated with the prevention of mitochondrial dysfunction and caspase activation. Thus, our results suggest that the inhibition of apoptosis by CsA may at least partly contribute to the anti‐inflammatory effect of CsA.