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目的探讨麦角甾醇对S180荷瘤小鼠抑瘤作用及机制。方法建立S180荷瘤小鼠模型,将50只荷瘤小鼠随机分为模型组、环磷酰胺组,高、中、低剂量麦角甾醇组,每组10只,雌雄各半;连续给药21 d,计算抑瘤率;苏木素-伊红染色,观察肿瘤组织生长情况;测定肝脏中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPx)活力和丙二醛(MDA)含量;Western blot法检测肿瘤组织中survivin蛋白表达。结果与模型组比较,环磷酰胺组、高、中、低剂量麦角甾醇组小鼠抑瘤率分别为53.96%、41.64%、29.90%、19.52%,差异均有统计学意义(P<0.05);各麦角甾醇组小鼠肿瘤组织内均出现不同程度微血管减少和多种凋亡形态学改变;与模型组比较,高、中剂量麦角甾醇组小鼠肝脏中SOD、GSH-Px活力[分别为(69.19±12.18)、(66.30±8.80)与(6 982.69±1 141.96)、(6414.43±932.96)U/mg prot]明显升高(P<0.05),MDA水平[分别为(24.59±6.87)、(31.43±7.05)nmol/mg prot]明显降低(P<0.05);与模型组比较,高、中剂量麦角甾醇组小鼠肿瘤组织中survivin蛋白表达水平下调(P<0.05)。结论麦角甾醇对S180荷瘤小鼠具有抑瘤作用,其机制可能与提高小鼠肝脏抗氧化能力和降低肿瘤组织中survivin蛋白表达水平有关。
Objective To investigate the antitumor effect and mechanism of ergosterol on S180 tumor-bearing mice. Methods S180 tumor-bearing mice model was established. Fifty tumor-bearing mice were randomly divided into model group, cyclophosphamide group, high, medium and low doses of ergosterol group, 10 in each group, male and female; continuous administration of 21 d, calculate the tumor inhibition rate; hematoxylin-eosin staining to observe the growth of tumor tissue; determination of liver activity of superoxide dismutase (SOD), glutathione peroxidase (GSHPx) activity and malondialdehyde (MDA) content Western blot was used to detect the expression of survivin protein in tumor tissue. Results Compared with the model group, the tumor inhibition rates of cyclophosphamide group were 53.96%, 41.64%, 29.90% and 19.52%, respectively, with significant difference (P <0.05) ; All ergosterol groups showed different degrees of microvessel density and morphological changes of apoptosis in all the groups; compared with the model group, the activity of SOD and GSH-Px in the liver of high and medium dose ergosterol-treated mice [ (69.19 ± 12.18), (66.30 ± 8.80) and (6 982.69 ± 1 141.96) and (6414.43 ± 932.96) U / mg prot] (31.43 ± 7.05) nmol / mg prot] (P <0.05). Compared with the model group, the expression of survivin protein in high and medium dose ergosterol group mice was down-regulated (P <0.05). Conclusion Ergosterol has anti-tumor effect on S180 tumor-bearing mice, and its mechanism may be related to improving liver anti-oxidation ability and reducing the expression of survivin in tumor tissue.