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目的 :探讨α-黑色素细胞刺激素对LPS部分生物学活性的影响。方法 :本文应用比色法、倒置生物显微镜及流式细胞仪观察小鼠腹腔巨噬细胞释放H2 O2 、中性粒细胞凋亡及FITC -LPS与单核细胞的结合情况。结果 :LPS可刺激小鼠腹腔巨噬细胞释放H2 O2 ,而α -MSH与LPS共同培养 ,则能明显抑制巨噬细胞释放H2 O2 (P <0 0 1) ;α-MSH及LPS本身均不影响中性粒细胞凋亡 (P >0 0 5 ) ,但在LPS作用下 ,α -MSH可显著促进中性粒细胞凋亡 (P <0 0 1) ;并且 ,α -MSH可降低FITC -LPS与单核细胞的结合率及单核细胞表面的平均荧光强度 (P <0 0 5 ,P <0 0 1)。结论 :α-MSH不仅能有效抑制LPS刺激巨噬细胞释放H2 O2 、促进LPS作用下的中性粒细胞发生凋亡 ;而且可干扰LPS与单核细胞的结合 ,发挥其有效的免疫调控作用。
Objective: To investigate the effect of α-melanocyte-stimulating hormone on some biological activities of LPS. Methods: The expression of H2O2, neutrophil apoptosis and the combination of FITC-LPS and monocytes in mouse peritoneal macrophages were observed by colorimetric method, inverted biomicroscopy and flow cytometry. Results: LPS stimulated the release of H2O2 from mouse peritoneal macrophages, while the co-culture of α-MSH and LPS significantly inhibited the release of H2O2 from macrophages (P <0.01); neither α-MSH nor LPS itself (P> 0.05). However, α-MSH could significantly promote neutrophil apoptosis under the action of LPS (P <0.01). Moreover, α-MSH could reduce the FITC- The binding rate of LPS to monocytes and the average fluorescence intensity of monocytes (P <0.05, P <0.01). CONCLUSION: α-MSH can not only effectively inhibit the LPS-stimulated macrophages from releasing H2O2, but also promote the apoptosis of neutrophils under the action of LPS. Moreover, it can interfere with the binding of LPS to monocytes and exert its effective immunomodulatory effects.