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Influence of gallic acid on porcine neutrophils phosphodiesterase 4, IL-6, TNF-α and rat arthritis model
- JIANG, Dai-xun, ZHANG, Mei-hua, ZHANG, Qian, CHEN, Yi-shan, MA, Wen-jing, WU, Wei-peng, MU, Xiang, CHEN, Wu
- Journal of integrative agriculture 2015 v.14 no.4 pp. 758-764
- Paeonia lactiflora, adjuvants, animal models, anti-inflammatory activity, arthritis, cyclic AMP, dose response, enzyme-linked immunosorbent assay, gallic acid, genes, high performance liquid chromatography, in vivo studies, inflammation, interleukin-6, neutrophils, quantitative polymerase chain reaction, rats, reverse transcriptase polymerase chain reaction, roots, swine, tumor necrosis factor-alpha
- Our previous studies showed that the anti-inflammatory effects of Paeonia lactiflora roots extract may be mediated, at least in part, through its gallic acid content, and this effect may be regulated in part by an inhibition on cAMP-phosphodiesterase (PDE). To explore the anti-inflammatory effect and mechanism, the influence of gallic acid on neutrophils PDE4 activity and expression, TNF-α and 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-α in supernatant were assayed by ELISA method. Model of rat arthritis was caused by complete Freund's adjuvant. Results showed that gallic acid had a dose-dependent restraint on PDE4 activity of neutrophils in vitro, promoted significantly PDE4A expression (P<0.01), and had no influence on the expressions of PDE4B and 4D. However, PDE4C expression was not detected. Gallic acid could promote IL-6 release (P<0.05), and inhibit TNF-α release of neutrophils (P<0.05). The experiment in vivo showed that gallic acid had obvious restraint on local inflammation of animal model (P<0.05). Therefore, the anti-inflammatory effect of gallic acid may be mediated in part through an inhibition on PDE4 activity and further an increase of IL-6 and a decrease of TNF-α of neutrophils, and this effect seemed to have no relationship with PDE4 expression.