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目的:探讨红景天多糖对宫颈癌U14模型小鼠的治疗作用及潜在机制。方法:分别采用腹腔及前肢腋下接种U14细胞建立小鼠U14腹水瘤及实体瘤模型,随机分为模型组、环磷酰胺(25 mg/kg)阳性对照组及红景天多糖低(75 mg/kg)、中(150 mg/kg)、高(300 mg/kg)剂量组,红景天多糖组灌胃给药,环磷酰胺组腹腔注射给药,1次/d,共10 d;检测各组U14腹水瘤小鼠生命延长率及U14实体瘤小鼠抑瘤率、脾脏指数、胸腺指数、脾淋巴细胞增殖能力及血清肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)和白细胞介素-2(IL-2)水平。结果:与模型组比较,各剂量红景天多糖均能显著延长U14腹水瘤小鼠平均存活天数,增加U14实体瘤小鼠抑瘤率及血清TNF-α、IFN-γ、IL-2水平和胸腺指数(P<0.05或P<0.01);红景天多糖中、高剂量组小鼠脾脏指数较模型组显著升高(P<0.05或P<0.01);与模型组比较,红景天多糖各量组小鼠脾淋巴细胞增殖能力在12、24、48 h三个时间点均显著升高(P<0.05或P<0.01)。结论:红景天多糖具有抑制宫颈癌U14模型小鼠肿瘤生长的作用,其机制与提高免疫力有关。
Objective: To investigate the therapeutic effect of Rhodiola polysaccharides on cervical cancer U14 model mice and its potential mechanism. Methods: U14 cells were inoculated intraperitoneally into the abdominal cavity and forelimb respectively to establish a model of U14 ascites tumor and solid tumor in mice, which were randomly divided into model group, positive control group of cyclophosphamide (25 mg / kg) and low polysaccharide of Rhodiola (75 mg (150 mg / kg) and high dose (300 mg / kg) of Rhodiola rosea polysaccharide group, intraperitoneal injection of cyclophosphamide group was given once a day for 10 days. The survival rate of mice in U14 ascites tumor and the tumor inhibition rate, spleen index, thymus index, proliferation of splenic lymphocytes and serum levels of tumor necrosis factor-α (TNF-α) and interferon-γ IFN-γ) and interleukin-2 (IL-2) levels. Results: Compared with the model group, Rhodiola rosea polysaccharide at various dosages could prolong the average survival time of U14 ascites tumor mice and increase the tumor inhibition rate and serum levels of TNF-α, IFN-γ and IL-2 in U14 solid tumor mice (P <0.05 or P <0.01). Compared with the model group, the spleen index of Rhodiola rosea polysaccharide group and high dose group was significantly higher than that of the model group (P <0.05 or P <0.01) The proliferation ability of splenic lymphocytes in all the groups was significantly increased at three time points (P <0.05 or P <0.01) at 12, 24 and 48 h. Conclusion: Rhodiola polysaccharides can inhibit the growth of U14 mouse model of cervical cancer, the mechanism of which is related to the enhancement of immunity.