目的:探讨茶藨子木层孔菌多糖硫酸酯(PRP-S)的体内抗肿瘤作用与机制。方法:建立小鼠H22实体瘤模型,分别给于高低剂量PRP-S,测定小鼠肿瘤生长抑制率、脾脏指数和胸腺指数;采用免疫组织化学法测定肿瘤组织中Bax、Bcl-2和b FGF蛋白表达;酶联免疫吸附实验法测定小鼠血清肿瘤坏死因子TNF-α的含量。结果:PRP-S10和PRP-S16在高剂量时对小鼠肿瘤的抑制率分别为54.6%和60.6%,与模型组比较有极显著性差异(P<0.01);并且对荷瘤小鼠的脾脏指数和胸腺指数没有明显影响;PRP-S10和PRP-S16均可以上调肿瘤组织中的促凋亡基因Bax、下调凋亡抑制基因Bcl-2的蛋白表达;PRP-S实验组小鼠血清TNF-α的含量显著高于模型组小鼠(P<0.01);PRP-S可以显著降低肿瘤组织中b FGF水平(P<0.01)。结论:PRP-S在抑制肿瘤的同时,免疫损伤不良反应小;其机制除促进细胞凋亡和肿瘤细胞坏死之外,还可能与抑制肿瘤的血管生成作用有关。 Objective: To investigate the antitumor effect and mechanism of Pseudomonas putida polysaccharide sulfate (PRP-S) in vivo. Methods: The H22 solid tumor model was established in mice. PRP-S was administered to the mice at low and high doses, respectively. The growth inhibition rate, spleen index and thymus index of mice were determined. The expressions of Bax, Bcl-2 and b FGF in tumor tissue were detected by immunohistochemistry The expression of TNF-α in serum was detected by enzyme-linked immunosorbent assay (ELISA). Results: The inhibitory rates of PRP-S10 and PRP-S16 on mice tumors were 54.6% and 60.6%, respectively, which were significantly different from those of the model group (P <0.01) Spleen index and thymus index had no significant effect; PRP-S10 and PRP-S16 could up-regulate the expression of Bax and Bcl-2 in tumor tissue; (P <0.01). PRP-S significantly decreased the level of b FGF in tumor tissue (P <0.01). CONCLUSIONS: PRP-S inhibits the tumor at the same time, the adverse reaction of immune damage is small. The mechanism of PRP-S may be related to the inhibition of tumor angiogenesis in addition to the promotion of apoptosis and tumor cell necrosis.