【摘要】 目的　研究c9,t11 共轭亚油酸 (CLA)对C5 7小鼠巨噬细胞杀伤黑色素瘤 (B16 MB)细胞能力的影响并探讨其可能机制。方法　用 0、2 5、5 0、75、10 0 μmol/LCLA处理巨噬细胞 2 4h后 ,分别用四甲基偶氮唑盐法检测CLA处理的巨噬细胞对B16 MB细胞的杀伤能力 ;逆转录聚合酶链式反应方法检测C5 7小鼠巨噬细胞细胞因子IL 6、TNF α和iNOSmRNA表达 ;免疫印迹法 (Westernblot)检测细胞外信号调节蛋白激酶 (Erk)的表达情况。结果　c9,t11 CLA处理后 ,巨噬细胞对肿瘤抑制率随剂量的升高而升高 ,同时 ,白细胞介素 (IL 6 )、肿瘤坏死因子 (TNF α)和一氧化氮合酶 (iNOS)mRNA表达增加 ;Erk的表达下降。结论　c9,t11 CLA增强C5 7小鼠巨噬细胞对B16 MB细胞的杀伤能力 ,并与其诱导IL 6、TNF α和iNOSmRNA的表达有关。推测CLA发挥抗肿瘤作用可能与其参与机体免疫调节作用有关 ,并且CLA对小鼠巨噬细胞IL 6的影响与促裂原活化蛋白激酶 细胞外信号调节蛋白激酶途径无关更多还原

【Abstract】 Objective To study the effects of c9,t11 conjugated linoleic acid on the killing ability of macrophage to B16 MB cells in C57 mice and explore its possible mechanism Methods The five levels of CLA was designed as 0,25,50,75,100 μmol/L After macrophage was treated with CLA for 24 h, the killing ability of macrophage on B16 MB cells was evaluated by MTT, The expression of C57 mice macrophage cytokine IL 6,TNF α and iNOS mRNA was detected by RT PCR The expression of Erk protein was examined by Western Blot assay Results The inhibitory effect of macrophage on tumor cell depend on the treatment of the increased c9,t11 CLA level, at the same time, the expression of IL 6,TNF α and iNOS mRNA increased, the expression of Erk decreased with the elevating dose of CLA. Conclusions c9,t11 CLA could increase the killing ability of macrophage in mice to B16 MB cells, and it was associated with induction of IL 6,TNF α and iNOS mRNA expression We speculate that antitumor ability of CLA may be associated with taking part in body immune regulation action, and the effects of CLA on the killing ability of murine macrophage to B16 MB cells was not associated with the MAPKErk pathway更多还原