菝葜乙酸乙酯部位对H22荷瘤小鼠的抑瘤作用及其机制研究

摘要

OBJECTIVE:To study the anti-tumor effects of ethyl acetate part of Smilaz china on H22 liver cancer-bearing mice and its mechanism. METHODS:90 mice were randomly divided into normal group,model group,positive control group (cytox-an,0.02 g/kg,ip,every 2 days)and ethyl acetate part of S. china low-dose,medium-dose and high-dose groups [1.0,2.0,4.0 g (crude drug)/kg,ig,twice a day]. Except for normal group,H22 transplanted models of mice were established. The next day after modelation,treatment groups were given relevant medicine,and normal group and model group were given constant volume of 0.5% sodium carboxymethylcellulose solution intragastrically. The change of body weight and tumor weight were observed after medication;the serum levels of VEGF and neoangiogenesis(NOS)were determined as well as vascular permeability of tumor;the expression of CD31 was detected in tumor tissue. RESULTS:Compared with model group,body weight and tumor weight of posi-tive control group were decreased significantly,while the serum levels of VEGF and NOS,vascular permeability of tumor were in-creased significantly(P<0.05 or P<0.01). Tumor weight and the expression of CD31 were decreased significantly in ethyl acetate part of S. china medium-dose and high-dose groups,while serum levels of VEGF and NOS,vascular permeability of tumor were in-creased significantly (P<0.05 or P<0.01). Tumor weight were decreased significantly in ethyl acetate part of S. china low-dose group,while vascular permeability of tumor was strengthened(P<0.05 or P<0.01). CONCLUSIONS:The ethyl acetate part of S. china shows anti-tumor effects in H22 liver cancer-bearing mice,and its mechanism might be associated with reducing the serum lev-els of VEGF and NOS,improving vascular permeability of tumor and inhibiting neovascularization.%目的：探讨菝葜乙酸乙酯部位对肝癌H22荷瘤小鼠的抑瘤作用及其机制。方法：将90只小鼠随机分为正常组、模型组、阳性对照组（环磷酰胺，0.02 g/kg，隔日ip给药1次）和菝葜乙酸乙酯部位低、中、高剂量组[1.0、2.0、4.0 g（生药）/kg，每天ig给药2次）。除正常组外，其余各组小鼠复制移植性实体瘤模型。造模次日，各给药组小鼠给予相应药物，正常组和模型组小鼠ig等体积0.5％羧甲基纤维素钠溶液，持续14 d。观察给药后小鼠体质量、瘤质量变化，测定小鼠血清中血管内皮生长因子（VEGF）、一氧化氮合酶（NOS）水平及瘤组织血管通透性，并检测瘤组织中血小板内皮细胞黏附分子1（CD31）表达水平。结果：与模型组比较，阳性对照组小鼠的体质量、瘤质量显著减少，血清中VEGF、NOS水平显著升高，瘤组织血管通透性显著增强（P＜0.05或P＜0.01）；菝葜乙酸乙酯部位中、高剂量组小鼠瘤质量显著减少，血清中VEGF、NOS水平显著升高，瘤组织的血管通透性显著增强、CD31表达水平降低（P＜0.05或P＜0.01）；菝葜乙酸乙酯部位低剂量组小鼠瘤质量明显减少，瘤组织血管通透性增强（P＜0.05或P＜0.01）。结论：菝葜乙酸乙酯部位对H22荷瘤小鼠有一定的抑瘤作用，其作用机制可能与降低荷瘤小鼠血清中VEGF与NOS水平、使肿瘤血管正常化和抑制肿瘤新生血管形成有关。