Cyclosporin A inhibits H2O2-induced apoptosis of human fibroblasts.
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 H2O2-induced apoptosis. Preincubation of human fibroblasts with CsA dose-dependently decreased H2O2-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.
Sugano
N
N
Nihon University School of Dentistry, Department of Periodontology, Tokyo, Japan. sugano-n@dent.nihon-u.ac.jp
Ito
K
K
Murai
S
S
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000378:metabolism; D002478:Cells, Cultured; D016572:Cyclosporine / Q000494:pharmacology*; D053938:DNA Fragmentation / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016572:Cyclosporine; D006861:Hydrogen Peroxide; D020169:Caspases