Effects of esculentoside A on production of interleukin-1, 2, and prostaglandin E2
Abstract
AIM:
To investigate the influence of esculentoside A (EsA) on immunological function and its mechanism of anti-inflammation.
METHODS:
Interleukin-1 production was measured by thymocyte co-stimulating assay; the radioactivity of [(3)H]arachidonic acid (AA) was used to evaluate the release of AA; prostaglandin E2 production was measured with radioimmunoassay (RIA); IL-2 and IFN-gamma were detected by ELISA method.
RESULTS:
EsA (3-12 micromol/L)could potently inhibit the production of IL-1 and PGE(2) from both silent and LPS induced macrophages. EsA had no significant effect on the release of AA from murine macrophages. EsA could inhibit the production of IL-2 from murine lymphocytes induced by ConA, but not affect the production from silent lymphocytes. EsA showed no effect on the production of IFN-gamma from both silent and ConA induced lymphocytes.
CONCLUSION:
EsA could affect the immunological function through inhibiting the production of IL-2 from activated splenocytes and the inhibition of production of IL-1 and PGE(2) might be one of the anti-inflammation mechanisms of EsA.
Keywords:
To investigate the influence of esculentoside A (EsA) on immunological function and its mechanism of anti-inflammation.
METHODS:
Interleukin-1 production was measured by thymocyte co-stimulating assay; the radioactivity of [(3)H]arachidonic acid (AA) was used to evaluate the release of AA; prostaglandin E2 production was measured with radioimmunoassay (RIA); IL-2 and IFN-gamma were detected by ELISA method.
RESULTS:
EsA (3-12 micromol/L)could potently inhibit the production of IL-1 and PGE(2) from both silent and LPS induced macrophages. EsA had no significant effect on the release of AA from murine macrophages. EsA could inhibit the production of IL-2 from murine lymphocytes induced by ConA, but not affect the production from silent lymphocytes. EsA showed no effect on the production of IFN-gamma from both silent and ConA induced lymphocytes.
CONCLUSION:
EsA could affect the immunological function through inhibiting the production of IL-2 from activated splenocytes and the inhibition of production of IL-1 and PGE(2) might be one of the anti-inflammation mechanisms of EsA.