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Objective:To determine the anti-inflammatory effects of an ethanol fraction of Periploca forrestii Schltr.(EFPF) and to investigate the potential mechanisms underlying in vivo and in vitro models. Methods:The antiinflammatory effects of EFPF were evaluated using the xylene-induced mouse ear edema and carrageenan-induced rat paw edema models in vivo. In vitro, RAW264.7 cells were exposed to 0–800 μg/m L EFPF and the cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. Then cells were treated with different concentrations of EFPF(100–400 μg/m L) and stimulated with lipopolysaccharide(LPS, 1 μg/m L) for 24 h. The supernatant was analyzed for nitric oxide(NO) using the Griess reagent, and the levels of inflammatory mediators and cytokines were determined using enzyme-linked immunosorbent assays for prostaglandin E2(PGE2), tumor necrosis factor α(TNF-α), interleukin(IL) 6, and IL-10. The protein expressions of inducible NO synthase(i NOS), cyclooxygenase-2(COX-2), nuclear factor κB(NF-κB), and mitogen-activated protein kinases(MAPKs) including extracellular signal-regulated kinase(ERK), c-Jun N-terminal kinase(JNK), and p38 MAPK were examined by Western blot. Results:Compared with the control group, EFPF significantly reduced mouse ear edema and rat paw edema rate(P<0.05 or P<0.01). Compared with the LPS group, EFPF significantly inhibited the LPS-stimulated production of NO, PGE2, TNF-α and IL-6(P<0.05 or P<0.01), and increased the IL-10 production(P<0.05). EFPF also significantly inhibited LPS-induced protein expressions of i NOS and COX-2, suppressed the phosphorylation and degradation of inhibitor of NF-κB-α, decreased p65 level, and inhibited the phosphorylation of p38, ERK1/2 and JNK(P<0.05 or P<0.01). Conclusion:EFPF exerted anti-inflammatory effect by reducing protein expressions of i NOS and COX-2 and the production of the inflammation factors, including TNF-α, IL-6, NO and PGE2, mainly through inhibition of LPS-mediated stimulation of NF-κB and MAPK signaling pathways.
Objective: To determine the anti-inflammatory effects of an ethanol fraction of Periploca for restii Schltr. (EFPF) and to investigate the potential mechanisms underlying in vivo and in vitro models. Methods: The antiinflammatory effects of EFPF were evaluated using the xylene- induced mouse Ear edema and carrageenan-induced rat paw edema models in vivo. In vitro, RAW264.7 cells were exposed to 0-800 μg / ml EFPF and the cell viability was determined by 3- (4,5-dimethylthiazol-2-yl ) -2,5-diphenyltetrazolium bromide (MTT) assay. Then cells were treated with different concentrations of EFPF (100-400 μg / mL) and stimulated with lipopolysaccharide (LPS, 1 μg / mL) was analyzed for nitric oxide (NO) using the Griess reagent, and the levels of inflammatory mediators and cytokines were determined using enzyme-linked immunosorbent assays for prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha), interleukin (IL) 6, and IL-10. The protein expressions of inducible NO syntha (COX-2), nuclear factor κB (NF-κB) and mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK were examined by Western blot. Compared with the control group, EFPF significantly reduced mouse ear edema and rat padedema rate (P <0.05 or P <0.01) inhibited the LPS-stimulated production of NO, PGE2, TNF-α and IL-6 (P <0.05 or P <0.01), and increased the IL- of i NOS and COX-2 suppressed the phosphorylation and degradation of inhibitor of NF-κB-α, decreased p65 level, and inhibited the phosphorylation of p38, ERK1 / 2 and JNK (P <0.05 or P <0.01) EFPF exerted anti-inflammatory effect by reducing protein expressions of iNOS and COX-2 and the production of the inflammation factors, including TNF-α, IL-6, NO and PGE2, mainly through inhibition of LPS-mediated stimulation of NF-κB and MAPK signaling pathways.