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目的探讨羟基磷灰石纳米粒子(Nano HAP)在体内对兔VX2肝种植瘤生长的抑制作用及对肿瘤细胞bax/bcl-2凋亡蛋白表达的影响。方法将56只VX2肝荷瘤兔随机分成四组,通过肝动脉灌注Nano HAP溶胶、5-Fu以及5-Fu与Nano HAP的混合液,并与生理盐水组对照。观察各组动物的一般情况,对肿瘤体积进行监测并比较。采用免疫组织化学染色观察bax/bcl-2蛋白的表达。结果各治疗组对肿瘤生长都有明显的抑制作用。Nano HAP溶胶组肿瘤体积明显小于对照组(P<0.05),肿瘤生长抑制率达到28.1%;5-Fu组抑瘤率达到43.7%,但动物表现出明显毒副作用;联合治疗组抑瘤率达到51.2%,而且毒副反应明显小于5-Fu组。Nano HAP组及联合治疗组免疫组织化学染色显示bcl-2蛋白表达率分别为41.7%(5/12)、38.5%(5/13),较对照组72.7%(8/11)明显降低;bax蛋白表达率为50.0%(6/12)、61.5%(8/13),明显高于对照组27.3%(3/11)。结论Nano HAP在体内对兔VX2肝种植瘤生长有明显的抑制作用,而且能明显降低5-Fu的毒性作用。其抑瘤机制可能是通过影响bax/bcl-2的表达加速肿瘤细胞凋亡。
Objective To investigate the inhibitory effect of hydroxyapatite nanoparticles (Nano HAP) on the growth of rabbit VX2 liver xenografts in vivo and its effect on the expression of bax / bcl-2 apoptotic protein in tumor cells. Methods Fifty-six VX2 hepatic tumor-bearing rabbits were randomly divided into four groups. Nano HAP sol, 5-Fu and a mixture of 5-Fu and Nano HAP were perfused through the hepatic artery and compared with saline group. The general situation of each group of animals was observed, the tumor volume was monitored and compared. Immunohistochemical staining was used to observe the expression of bax / bcl-2 protein. Results The treatment groups have obvious inhibitory effect on tumor growth. The tumor volume of Nano HAP sol group was significantly lower than that of control group (P <0.05), and the tumor growth inhibition rate reached 28.1%. The inhibition rate of 5-Fu group reached 43.7%, but the animals showed obvious toxic and side effects. 51.2%, and the side effects were significantly less than the 5-Fu group. The expression of bcl-2 protein in Nano HAP group and combined treatment group was 41.7% (5/12), 38.5% (5/13), respectively, which was significantly lower than that in control group (72.7%, 8/11) The protein expression rate was 50.0% (6/12), 61.5% (8/13), significantly higher than the control group 27.3% (3/11). Conclusion Nano HAP significantly inhibits the growth of rabbit VX2 liver xenografts in vivo and can significantly reduce the toxicity of 5-Fu. The anti-tumor mechanism may be through the impact of bax / bcl-2 expression accelerated tumor cell apoptosis.