摘要
目的:研究黄芪多糖(APS)的抗肿瘤作用及其机制。方法:采用小鼠肝癌HepA移植瘤的动物模型,以瘤重抑制率为指标。体外采用人肝癌Bel-7404细胞,用四甲基偶氮唑盐(MTT)法或3H-胸腺嘧啶([3H]TdR)掺入法测肿瘤细胞生长。放免法和ELISA法检测TNF-α和IFN-γ。结果:APS显著抑制小鼠肝癌HepA的生长;体外对Bel-7404细胞没有抑制作用,但APS与小鼠PMΦ或脾细胞共培养上清对Bel-7404细胞的生长具有显著抑制作用。APS(160,320和640mg.L-1)使正常的小鼠PMΦ培养上清中TNF-α的活性升高。APS(160,320和640mg.L-1)明显增加正常小鼠脾细胞培养上清中IFN-γ的产生。结论:APS无直接抗肿瘤作用,其抗肿瘤作用是通过促进TNF-α和IFN-γ的产生而实现的。
OBJECTIVE To study the antitumor activity of astragalus polysaccharide （APS） and its mechanism of action. METHODS By using experimental model of hepatoma （HepA） in mice, the inhibitory effect of tumor weight of APS on the growth of HepA tumor cells in mice was tested. The cytotoxic effect of APS on Bel-7404 cells in vitro was detected by MTT assay or [^3H]TdR incorporation methods. TNF-α and IFN-γ were measured by radioimmunoreagent kit and ELISA kit. RESULTS APS inhibited the growth of HepA tumor cells in mice. But APS had no direct inhibitory effect on the growth of Bel-7404 cells. The cultural supernatants of peritoneal macrophages or splenocytes treated with APS（160,320 and 640 mg·L^-1 ）had remarkable inhibitory effect on the growth of Bel-7404 cells. APS increased TNF-α production of PMφ and IFN-γ production of spleenocytes. CONCLUSION APS can inhibit the growth of tumor cells of HepA in mice. The antitumor activity of APS is obtained via its immunopetenting effect such as promoting release of TNF-α and IFN-γ.
出处
《中国医院药学杂志》
CAS
CSCD
北大核心
2005年第10期923-925,共3页
Chinese Journal of Hospital Pharmacy
