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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。
Colchicine (Col.), A microtubule polymerization inhibitor, can dose-dependently inhibit the secretion of TNF-α by LPS-stimulated rat macrophages (Mψ). Co-derivatives β-lumicolchicine had no effect on microtubules and had no effect on the secretion of TNF-α; other microtubule inhibitors such as vincristine also inhibited Mψ secretion of TNF-α. Indirect immunofluorescence staining and in situ hybridization showed that LPS could promote microtubule polymerization and significantly increase the expression of TNF-αmRNA and protein. When LPS and Col. In combination, microtubule depolymerization, TNF-αmRNA expression and protein synthesis decreased. TNF-α lost its original cytoplasmic localization and dispersed in the cytoplasm. These results indicate that the synthesis of TNF-α requires intact microtubule structure and function, and suggests that changes in microtubule function under physiological or pathological conditions may be directly or indirectly involved in the regulation of TNF-α biosynthesis.