Objective To investigate the potential role of Lycium bararum polysaccharide (LBP) with or without interferon -inducible protein 10 ( CXCL10) in inducing dendritic cells ( DC) functional maturation by monitoring the alteration of cytokines for inducing DC maturation in peripheral blood and by detecting the expression of S-100 protein in tumor tissue, thus to reveal its mechanism of inhibiting experimental liver cancer. Methods H22 bearing mice model was established. The mice were randomized into model group, LBP group (50 mg/kg, ig), CXCL10 (right axillary subcutaneous injection of 15 μg/kg), LBP + CXCL10 group (LBP 50 mg/kg, ig, and right axillary subcutaneous injection of CXCL10 15 μg/kg), 5- fluorouracil (5FU) group ( intraperitoneal injection of 12mg/kg) , 12 mice in each group. The mice were administered the corresponding medicine once a day. After treatment for 2 continuous weeks, blood was sampled from infraorbital vein, and the tumor mass, spleen, thymus were extracted for the calculation of anti-tumor rate, thymus index and spleen index separately . The mRNA expression levels of interleukin 12 (IL-12) and tumor necrosis factor-α (TNF-α) in peripheral blood were detected by fluorescence quantitative PCR, the expression of S-100 protein in tumor tissues was detected by immunohistochemical assay. Results Compared with the model group, tumor growth in LBP group and LBP+CXCL10 group was obviously inhibited, and tumor-inhibitory rate was 55.90%, 50.91%, respectively. Meanwhile, the mRNA expression level of IL-12 was 2.94 folds higher in LBP group and 3.39 folds higher in LBP + CXCL10 group, and TNF-α mRNA expression level was 1.55 folds higher in LBP group and 4.74 folds higher in LBP+CXCL10 group than the model group, the differences being statistical significant ( P<0.05 or P<0.01). Results of immunohistochemical assay showed that S-100+DC number in LBP group and LBP+CXCL10 group was larger than that in the model group (P<0.05 ). Conclusion LBP and LBP+CXCL10 exert significant effect on inhibiting experimental liver cancer. The mechanism may be related with inducing the secretion of IL-12 and TNF-α, which plays a key role in inducing DC maturation, and with the increase of the number of DC in tumor microenvironment.%【目的】检测外周血诱导树突状细胞（dendritic cells， DC）功能成熟的关键性细胞因子水平变化以及肿瘤组织S－100蛋白表达情况，探讨枸杞多糖（LBP）单用或联合CXC趋化因子配体10（CXCL10）对DC功能成熟潜在的影响，进一步揭示LBP抗实验性肝癌的作用机制。【方法】建立H22荷瘤小鼠模型，随机分为模型组、 LBP （50 mg／kg灌胃）组、 LBP ＋CXCL10（50 mg／kg灌胃＋15μg／kg右胁皮下注射）组、 CXCL10（15μg／kg右胁皮下注射）组、5-氟尿嘧啶（5－FU，12 mg／kg腹腔注射）组，每组12只。每天给药1次，连续2周后眼球取血，分离小鼠肿瘤、脾脏、胸腺，计算肿瘤抑制率、脾脏指数及胸腺指数。采用荧光定量PCR技术检测外周血白细胞介素－12（IL-12）及肿瘤坏死因子－α（TNF－α） mRNA表达，免疫组织化学法检测S－100蛋白在肿瘤间质浸润DC的表达。【结果】与模型组比较， LBP组及LBP＋CXCL10组对肿瘤生长具有明显的抑制作用，肿瘤抑制率分别达到55．90％、50．91％，且能显著提高外周血IL-12、 TNF－αmRNA表达， IL－12表达分别上调了2．94、3．39倍， TNF－α分别上调1．55、4．74倍，差异均有统计学意义（P＜0．05或P＜0．01）；免疫组织化学检查结果显示LBP组及LBP＋CXCL10组S－100＋DC数量显著高于模型组（P＜0．05）。【结论】 LBP及LBP＋CXCL10具明显的抗实验性肝癌作用，其作用机制与诱导DC功能成熟的关键性细胞因子IL－12、 TNF－α分泌，增加肿瘤微环境的DC数量有关。
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