LAUSR

The current study was designed to investigate the potential anti‐inflammatory and antioxidant effects of fingolimod against Ovalbumin (Ova)‐induced allergic airway inflammation compared to dexamethasone. Fingolimod was given (0.5 mg/kg/day, p.o.) for sensitized mice 1 h before Ova challenge from Days 19 to 24. Fingolimod significantly inhibited Ova‐induced elevation of inflammatory cells and eosinophils numbers in bronchoalveolar lavage fluid (BALF) and reduced concentrations of immunoglobulin E in serum and of sphingosine‐1‐phosphate, interleukin (IL)‐4, and IL‐13 in BALF. Fingolimod inhibited microvascular leakage and edema as reflected by the decreased lung/body weight index. These findings were supported by histopathological examination results showing that fingolimod substantially decreased perivascular edema and inflammatory cell infiltration. Fingolimod also attenuated Ova‐induced oxidative stress as evidenced by decreased malondialdehyde concentration along with increasing concentrations of reduced glutathione and superoxide dismutase in lung tissues. Fingolimod also significantly decreased monocyte chemoattractant protein‐1 (MCP‐1), p‐ERK, and p‐P38 in lung tissues of Ova‐challenged mice. In conclusion, the current study demonstrated the anti‐inflammatory and antioxidant effects of fingolimod in allergic airway inflammation that might be associated with the downregulation of mitogen activated kinases signaling to decrease T helper 2 cytokine secretion (IL‐4 and IL‐13) and MCP‐1 expression, along with the inhibition of oxidative stress.