Cyclosporin A inhibits H2O2-induced apoptosis of human fibroblasts.

Abstract

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.

• Authors: N Sugano, K Ito, S Murai
• Journal: FEBS letters (FEBS Lett) Vol. 447 Issue 2-3 Pg. 274-6 (Mar 26 1999) ISSN: 0014-5793 [Print] England
• PMID: 10214960 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents, Non-Steroidal
• Cyclosporine
• Hydrogen Peroxide
• Caspases

Topics

• Anti-Inflammatory Agents, Non-Steroidal (pharmacology)
• Apoptosis (drug effects)
• Caspases (metabolism)
• Cells, Cultured
• Cyclosporine (pharmacology)
• DNA Fragmentation (drug effects)
• Enzyme Activation (drug effects)
• Fibroblasts (cytology, drug effects, metabolism)
• Humans
• Hydrogen Peroxide (pharmacology)
• Mitochondria (drug effects, metabolism)