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目的:探讨六月青多糖对S180荷瘤小鼠免疫功能及凋亡基因p53,B细胞淋巴瘤/白血病-2(Bcl-2),多肽抗原(Bax)表达的影响。方法:将50只小鼠于右腋皮下接种S180腹水肿瘤细胞建立S180荷瘤模型,造模24 h后随机分为5组:模型(生理盐水20 mL.kg-1.d-1)组,环磷酰胺(0.02 g.kg-1.d-1)组,六月青多糖高、中、低剂量(分别为1.2,0.6,0.3 g.kg-1.d-1)组。除环磷酰胺组隔天ip给药外,余均ig给药10 d。停药24 h后检测荷瘤小鼠抑瘤率、胸腺系数和脾脏系数;MTT法检测ConA刺激脾淋巴细胞转化功能;中性红法检测腹腔巨噬细胞吞噬功能;免疫组织化学法检测肿瘤组织中p53,Bcl-2,Bax蛋白。结果:六月青多糖高剂量(1.2 g.kg-1.d-1)抑瘤率达38%;与模型组比较,六月青多糖各剂量组胸腺系数显著增高(P<0.05),高、中剂量组脾脏系数、脾淋巴细胞刺激指数和腹腔巨噬细胞吞噬功能显著增高(P<0.01或P<0.05);六月青多糖各剂量组p53表达无明显差异;高剂量组Bcl-2表达显著减弱(P<0.05)而Bax表达明显增强(P<0.05)。结论:六月青多糖能抑制小鼠S180肿瘤生长,其机制与增强S180荷瘤小鼠免疫功能、下调Bcl-2蛋白及上调Bax蛋白的表达有关。
Objective: To investigate the effect of polysaccharides from Junyou on immune function and expression of p53, Bcl-2 and Bax in S180 tumor-bearing mice. Methods: Fifty mice were inoculated subcutaneously into S180 ascites tumor cells in the right axilla to establish S180 tumor-bearing model. After 24 h, models were randomly divided into 5 groups: model (saline 20 mL.kg-1.d-1) Cyclophosphamide (0.02 g.kg-1.d-1) group, high, medium and low doses of polysaccharides (1.2,0.6,0.3 g.kg-1.d-1) group. In addition to cyclophosphamide ip administration group, Yu Jun ig administration for 10 days. Tumor inhibition rate, thymus coefficient and spleen coefficient of tumor-bearing mice were detected 24 h after drug withdrawal. ConA-stimulated splenic lymphocyte transformation was detected by MTT assay. Phagocytosis of peritoneal macrophages was detected by neutral red assay. In p53, Bcl-2, Bax protein. Results: Compared with the model group, the thymus coefficient of the polysaccharides in June was significantly higher (P <0.05) and the highest (P <0.01 or P <0.05). There was no significant difference in the expression of Bcl-2 in the high dose group (P <0.01 or P <0.05) The expression of Bax was significantly decreased (P <0.05) and the expression of Bax was significantly increased (P <0.05). Conclusion: The polysaccharide of Junyou can inhibit the growth of S180 tumor in mice. Its mechanism is related to the enhancement of immune function, down-regulation of Bcl-2 protein and up-regulation of Bax protein in S180 tumor-bearing mice.