Ariga T, Kiso M, Hasegawa A, Miyatake T
Clinical Research Center, Eisai Co. Ltd., Tokyo, Japan.
J Mol Neurosci. 2001 Dec;17(3):371-7. doi: 10.1385/JMN:17:3:371.
Amyloid-beta protein (A beta) is known to induce microglial activation with concomitant release of cytokines. Gangliosides have documented neuritogenic and neurotrophic properties. We determined the effects of A beta on the release of interleukin-1beta (IL-1beta) from the human monocytic cell line, THP-1 cells. A beta 1-42 significantly induced the release of IL-1beta from the cells. A beta 1-40, A beta 40-1, A beta 1-38, and A beta precursor protein (beta-APP) analogs also released a small amount of IL-1beta. A beta 1-42-activated cells demonstrated approx an 18-fold higher IL-1beta release than that for control cells or A beta 1-40 (soluble; S) treated cells. The release of IL-1beta from A beta 1-42-activated cells was significantly inhibited (33-48% of activated cells; p < 0.05 for the control value) by addition of gangliosides, suggesting that gangliosides inhibit the continuous cycle of the IL-1beta production in THP-1 cells.
已知β-淀粉样蛋白（Aβ）可诱导小胶质细胞活化并伴随细胞因子释放。神经节苷脂具有促神经突生长和神经营养特性。我们确定了Aβ对人单核细胞系THP-1细胞白细胞介素-1β（IL-1β）释放的影响。Aβ1-42显著诱导细胞释放IL-1β。Aβ1-40、Aβ40-1、Aβ1-38和Aβ前体蛋白（β-APP）类似物也释放少量IL-1β。Aβ1-42激活的细胞与对照细胞或Aβ1-40（可溶性；S）处理的细胞相比，IL-1β释放量高出约18倍。添加神经节苷脂可显著抑制Aβ1-42激活细胞释放IL-1β（占激活细胞的33%-48%；与对照值相比p<0.05），这表明神经节苷脂可抑制THP-1细胞中IL-1β产生的持续循环。
