Inlfuence of gallic acid on porcine neutrophils phosphodiesterase 4, IL-6, TNF-αand rat arthritis model

摘要

Our previous studies showed that the anti-inlfammatory effects of Paeonia lactilfora roots extract may be mediated, at least in part, through its gal ic acid content, and this effect may be regulated in part by an inhibition on cAMP-phosphodiesterase (PDE). To explore the anti-inlfammatory effect and mechanism, the inlfuence of gal ic acid on neutrophils PDE4 activity and expression, TNF-αand IL-6 content and rat arthritis model were further studied. PDE4 activity and gene express were calculated respectively by substrate cAMP change examined with HPLC and real-time RT-PCR. The concentration of IL-6 and TNF-αin supernatant were assayed by ELISA method. Model of rat arthritis was caused by complete Freund’s adjuvant. Results showed that gal ic acid had a dose-dependent restraint on PDE4 activity of neutrophils in vitro, promoted signiifcantly PDE4A expression (P<0.01), and had no inlfuence on the expressions of PDE4B and 4D. However, PDE4C expression was not detected. Gal ic acid could promote IL-6 release (P<0.05), and inhibit TNF-αrelease of neutrophils (P<0.05). The experiment in vivo showed that gal ic acid had obvious restraint on local inlfammation of animal model (P<0.05). Therefore, the anti-inlfammatory effect of gal ic acid may be mediated in part through an inhibition on PDE4 activity and further an in-crease of IL-6 and a decrease of TNF-αof neutrophils, and this effect seemed to have no relationship with PDE4 expression.