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PGE_23×10~(-7)～3×10~(-6)mol/L及硝苯吡啶5×10~(-6)～1×10~(-5)mol/L对ConA诱导的淋巴细胞增殖有明显抑制作用。药物作用48h后洗去药物,加入致裂原后继续培养细胞,结果发现硝苯吡啶的抑制作用已完全逆转,而PGE_23×10~(-6)mol/L的抑制作用则部分逆转。当低浓度PGE_2(3×10~(-3)mol/L)与硝苯吡啶(1×10~(-6)mol/L)同时作用于脾细胞时,可见两者作用正巧相加,无明显拮抗与协同作用。PGE_26×10~(-6)mol/L及硝苯吡啶1×10~(-5)mol/L对巨噬细胞移动有直接抑制作用。用~(51)Cr标记调理的绵羊红细胞方法证明低浓度PGE_2对巨噬细胞吞噬功能有增强,而硝苯吡啶预培养对吞噬功能影响不大。
PGE_ (23 × 10 ~ (-7) ~ 3 × 10 ~ (-6) mol / L and nifedipine 5 × 10 ~ (-6) ~ 1 × 10 ~ (-5) mol / L) Proliferation has a significant inhibitory effect. After 48h, the drugs were washed away and the cells were cultured after the addition of fission. The inhibition of nifedipine was completely reversed. However, the inhibitory effect of PGE23 × 10 -6 mol / L partially reversed. When splenocytes were treated with low concentrations of PGE 2 (3 × 10 -3 mol / L) and nifedipine (1 × 10 -6 mol / L), the two effects coincided with each other. Obvious antagonism and synergy. PGE 26 × 10 -6 mol / L and nifedipine 1 × 10 -5 mol / L could directly inhibit macrophage migration. The method of ~ (51) Cr-labeled sheep erythrocytes proved that the low concentration of PGE 2 enhanced the phagocytosis of macrophages, while the nifedipine pre-culture had little effect on phagocytosis.