α-MSH对脂多糖部分生物学活性的影响

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H₂O₂、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H2O2,而α-MSH与LPS共同培养,则能明显抑制巨噬细胞释放H₂O₂(P<0.01);α-MSH及LPS本身均不影响中性粒细胞凋亡(P>0.05),但在LPS作用下,α-MSH可显著促进中性粒细胞凋亡(P<0.01);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<0.05,P<0.01)。结论:α-MSH不仅能有效抑制LPS刺激巨噬细胞释放H₂O₂、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。

Effects of α-MSH on biological activities of LPS

AIM: The present study was undertaken to explore the effects of α-MSH on partial biological activities of LPS. METHODS:Colorimetric method was used for the measurement of hydrogen peroxide(H₂O₂) production in mouse peritoneal macrophages, the apoptosis of polymorphonuclear leukocytes(PMNs) and the binding of LPS to monocytes were studied with flow cytometry. RESULTS: It was found that LPS strongly stimulated macrophages to release H₂O₂. When macrophages were cultured with α-MSH in the presence of LPS, the H₂O₂ release was markedly suppressed (P<0.01). Neither LPS nor α-MSH alone was capable of affecting the apoptosis of PMNs (P>0.05). In the presence of LPS, however, α-MSH significantly promoted the apoptosis of PMNs (P<0.01). α-MSH significantly inhibited the binding of LPS to monocytes as the binding rate of FITC-LPS and the mean surface fluorescence intensity of monocytes ( P<0.05 and P<0.01, respectively). CONCLUSION: In the presence of LPS, α-MSH not only effectively suppressed the release of H₂O₂ from macrophages , promoted the apoptosis of PMNs, but also interfered with the binding of LPS to monocytes. α-MSH may play an important role in the immunomodulation of the body .