摘要
微管聚合抑制剂秋水仙碱（Ｃｏｌｃｈｉｃｉｎｅ，Ｃｏｌ．）能剂量依赖性地抑制ＬＰＳ刺激的大鼠巨噬细胞（Ｍψ）分泌ＴＮＦ－α。Ｃｏ１的衍生物β－ｌｕｍｉｃｏｌｃｈｉｃｉｎｅ对微管无影响，对ＴＮＦ－α的分泌亦无影响；其他微管抑制剂如长春新碱等亦能抑制Ｍψ分泌ＴＮＦ－α。间接免疫荧光染色和原位杂交法显示，ＬＰＳ能促进微管聚合，并使ＴＮＦ－αｍＲＮＡ及蛋白质表达明显增加；当ＬＰＳ与Ｃｏｌ．联用时，微管解聚，ＴＮＦ－αｍＲＮＡ表达及其蛋白质合成减少，ＴＮＦ－α失去原有的胞浆定位，弥散分布于胞浆。说明ＴＮＦ－α的合成需要完好的微管结构与功能，并提示在生理或病理条件下微管功能的变化可能直接或间接参与对ＴＮＦ－α生物合成的调节。
Microtubule polymerization inhibiting agent Col. chicine(Col.)was
found to depress dose-dependently the secretion of TNF-α by
LPS-stimulated rat macrophages (Mψs ).β-lumi Col.chicine,a
chemically closely related derivative of Col.,which showed no effect
on microtubulefunction, was found not to affect TNF-αsecretion as
well. Other microtubule inhibiting agents,including vinblasitne,could
also depress TNF-α secretion by LPS-stimulated Mψs. As shown
byindirect immunofluorescence and in situ hybridization LPS was able
to promote microtubulepolymerization and markedly increase the
intracellular TNF-α mRNA as well as the expressionof TNF-α protein.
Concomitant application of LPS and Col. led to disruption of
microtubulesand a decrease in TNF-α mRNA and TNF-α protein
expression. In cells treated with both LPSand Col.,TNF-α was found
to have lost its normal cytoplasmic lacalization and
dispersethroughout the cytoplasm. The mechanisms underlying the
Col,effect were discussed.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
1995年第2期70-74,共5页
Chinese Journal of Immunology
