Objective: To evaluate the anti-inflammatory effects of icariin, from aspects of pro-inflammatory cytokines, inflammatory mediators and adhesion molecules.
Methods: Mouse inflammation model in vitro was established by stimulating macrophage cell line RAW264. 7 with lipopolysaccharide (LPS); and the inflammation model in vivo was established by stimulating C57BL/6J mouse with LPS. Taking dexamethasone as the positive control, both models were treated with icariin, and the cell viability in model mice was detected with CCK-8 kit; tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) in cell culture medium and serum were detected by ELISA; nitric oxide (NO) in cell culture medium by Griess Reagent method; CD11b expression on the surface of neutrophil in mice by flow cytometry, and pulmonary inflammatory cell infiltration in mice by pathological section as well.
Results: in vitro studies showed that icariin at the doses of 1 microg/mL, 10 microg/mL and 100 microg/mL, all displayed no cytotoxicity (P < 0.01); 10 microg/mL and 100 microg/mL icariin effectively lowered the levels of TNF-alpha and IL-6 (P < 0.01) in medium; and 100 microg/mL icariin significantly reduced level of NO (P < 0.01) in medium. in vivo studies showed that icariin at the dose of 20 mg/kg significantly lowered serum TNF-alpha and IL-6 levels (P < 0.01), reduced the average fluorescence intensity of adhesion molecules CD11b (P < 0.01), and alleviated pulmonary inflammatory cell infiltration.
Conclusion: Icariin is a safe and effective natural anti-inflammatory drug, its partial mechanism is possible the multiple links intervention on pro-inflammatory cytokines (TNF-alpha, IL-6), inflammatory mediators (NO) and adhesion molecules (CD11b).