Antinociceptive activity of the S1P-receptor agonist FTY720

Antinociceptive activity of the S1P-receptor agonist FTY720

FTY720 is a novel immunosuppressive drug that inhibits the egress of lymphocytes from secondary lymphoid tissues and thymus. In its phosphorylated form FTY720 is a potent S1P receptor agonist. Recently it was also shown that FTY720 can reduce prostaglandin synthesis through the direct inhibition of the cytosolic phospholipase A2 (cPLA2). Since prostaglandins are important mediators of nocicepti...

The S1P receptor modulator FTY720 prevents the development of experimental colitis in mice.

To evaluate the therapeutic effects of the new synthetic sphingosine-1-phosphate (S1P) receptor modulator, FTY720, we investigated how FTY720 affects the development of dextran sulfate sodium (DSS)-induced colitis and CD4+CD62L+ T cell transfer colitis. BALB/c mice were fed a chow containing 3.5% (wt/wt) DSS to induce colitis. The CD4+CD62L+ T cell transfer colitis was induced by an intraperito...

Capsazepine, a Transient Receptor Potential Vanilloid Type 1 (TRPV1) Antagonist, Attenuates Antinociceptive Effect of CB1 Receptor agonist, WIN55,212-2, in the Rat Nucleus Cuneiformis

Introduction: Nucleus cuneiformis (NCF), as part of descending pain inhibitory system, cooperates with periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) in supraspinal modulation of pain. Cannabinoids have analgesic effects in the PAG, RVM and NCF. The transient receptor potential vanilloid type 1(TRPV1) can be activated by anandamide and WIN55,212-2 as a cannabinoid receptor ago...

Sequestration of CD4 Agonist FTY720 Differentially Affects the The Sphingosine 1-Phosphate Receptor

Cigarette smoke inhibits efferocytosis via deregulation of sphingosine kinase signaling: reversal with exogenous S1P and the S1P analogue FTY720.

Alveolar macrophages from chronic obstructive pulmonary disease patients and cigarette smokers are deficient in their ability to phagocytose apoptotic bronchial epithelial cells (efferocytosis). We hypothesized that the defect is mediated via inhibition of sphingosine kinases and/or their subcellular mislocalization in response to cigarette smoke and can be normalized with exogenous sphingosine...