NSAIDs increase GM-CSF release by human synoviocytes: comparison with nitric oxide-donating derivatives.

Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat the condition of rheumatoid arthritis, where levels of prostaglandin E2 (PGE2) and granulocyte macrophage-colony stimulating factor (GM-CSF) are elevated in the synovial fluid. NO-NSAIDs are a new class of cyclooxygenase (COX)-inhibitors developed by coupling a nitric oxide (NO)-donating moiety to conventional NSAIDs. We show that, in cytokine-treated synoviocytes (from non-rheumatic patients), NO-naproxen and NO-flurbiprofen like their parent compounds concentration-dependently reduce the levels of PGE2 (an index of COX-2 activity), with a corresponding rise in the release of GM-CSF.

Modulation by colony stimulating factors of human epithelial colon cancer cell apoptosis.

Colony stimulating factors (CSF) promote leukocyte survival by reducing apoptotic cell death. However, their effects on non-leukocyte cell types are unclear. Reduced apoptosis in colon epithelial cells is thought to contribute to the initiation of cancer.