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Objective:To study the effects of paclitaxel on macrophage activation.Methods:Mouse macrophages were isolated by peritoneal lavage and cultured in RPMI 1640 medium according to the following groups:paclitaxel(5μmol/L) group,IFN-γ(5U/L) group,paclitaxel (5μmol/L) and IFN-γ (5U/L) combination group, and control group(without paclitaxel and IFN-γ).24 hours later,supernatants were collected for nitric oxide(NO) assessment using the Griess reagent, and tumor necrosis factor-α(TNF-α) assessment using the enzyme linked immunosorbent assay.Antibody-dependent cell-mediated cytotoxicity(ADCC) of the macrophages was assessed using the method of hemoglobin-enzyme release assay (Hb-ERA).Results:Paclitaxel induced the production of higher levels of NO(8.86±1.16μmol/L) and TNF-α(120.2±10.2pg/ml),and enhanced the ADCC of macrophages[(20.61±1.13)%].The differences were significant compared with the control group[no NO and TNF-α detected,ADCC (15.37±1.93)%](P<0.01).Paclitaxel and IFN-γ in combination induced the production of higher levels of NO(22.85±0.91μmol/L) and TNF-α(358.6±27.5pg/ml),and enhanced the ADCC of macrophages[(42.49±3.09)%].The differences were significant compared with paclitaxel or IFN-γ[NO 8.09±1.13μmol/L,TNF-α 124.8±9.6pg/ml,ADCC (23.32±2.63)%] alone(P<0.01).Conclusion:These findings indicate that paclitaxel can promote NO and TNF-α production,enhance ADCC of macrophages,and induce macrophage activation.The active effects are more significant with paclitaxel and IFN-γ combination.
Objective: To study the effects of paclitaxel on macrophage activation. Methods: Mouse macrophages were isolated by peritoneal lavage and cultured in RPMI 1640 medium according to the following groups: paclitaxel (5 μmol / L) group, IFN- γ , paclitaxel (5 μmol / L) and IFN-γ (5 U / L) combination group, and control group (without paclitaxel and IFN- γ) .24 hours later, supernatants were collected for nitric oxide (NO) assessment using the Griess reagent, and tumor necrosis factor-α (TNF-α) assessment using the enzyme linked immunosorbent assay. Antibody-dependent cell-mediated cytotoxicity (ADCC) of the macrophages was assessed using the method of hemoglobin-enzyme release assay (Hb-ERA) : Paclitaxel induced the production of higher levels of NO (8.86 ± 1.16 μmol / L) and TNF-α (120.2 ± 10.2 pg / ml), and enhanced the ADCC of macrophages [(20.61 ± 1.13)%] compared with the control group [no NO and TNF-α detected, ADCC (15.37 ± 1.93)%] (P <0.01) .Paclitaxel and IFN-γ in The combination of the production of higher levels of NO (22.85 ± 0.91 μmol / L) and TNF-α (358.6 ± 27.5 pg / ml), and enhanced the ADCC of macrophages [(42.49 ± 3.09)%] with paclitaxel or IFN-γ [NO 8.09 ± 1.13 μmol / L, TNF-α 124.8 ± 9.6 pg / ml, ADCC (23.32 ± 2.63)%] alone (P <0.01) .Conclusion: These findings indicate that paclitaxel can promote NO and TNF-α production, enhance ADCC of macrophages, and induce macrophage activation. The active effects are more significant with paclitaxel and IFN-γ combination.