目的:研究新藤黄酸(neo-gambogic acid,NGA)对Hep G2裸小鼠移植瘤的体内抗肿瘤作用及其机制。方法:采用Hep G2裸小鼠移植瘤模型,造模7 d后将模型动物随机分为5组,即荷瘤对照组,阳性对照组(5-FU 10.0 mg.kg-1),NGA高、中、低剂量组(分别为8.0,4.0,2.0 mg.kg-1),隔天ip给药1次,给药7次后处死动物,分离肿瘤,测量肿瘤体积,称瘤重,计算相对肿瘤体积和抑瘤率,并将肿瘤组织切片,采用免疫组化法,检测实体瘤组织的Bax,Bcl-2,p-ERK1/2,p-MEK1/2蛋白的表达情况。结果:NGA高、中、低剂量组的平均瘤重[分别为(0.21±0.07),(0.41±0.17),(1.00±0.28)g]均明显低于荷瘤对照组(1.29±0.24)g,NGA高剂量组的抑瘤率为83.75%,高于阳性对照药5-FU的抑瘤率46.54%(P<0.05);Bax表达量呈剂量依赖性升高,Bcl-2表达量呈剂量依赖性降低;NGA给药组p-ERKl/2和p-MEKl/2的表达量均明显低于荷瘤对照组(P<0.05)。结论:NGA对Hep G2裸小鼠移植瘤具有确切的体内抗肿瘤作用,其作用机制与上调Bax/Bcl-2比值而诱导实体瘤细胞凋亡及下调丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号转导通路的磷酸化水平密切相关。 Objective: To study the antitumor effect and mechanism of neo-gambogic acid (NGA) on Hep G2-xenografted nude mice in vivo. Methods: The model of Hep G2 tumor-bearing mice was established. After 7 days of modeling, the model animals were randomly divided into 5 groups: tumor-bearing control group, positive control group (5-FU 10.0 mg.kg-1), high NGA, Medium and low dose groups (8.0,4.0,2.0 mg.kg-1, respectively), administered ip once every other day, administered 7 times and then sacrificed, the tumor was separated, the tumor volume was measured, the tumor weight was calculated, and the relative tumor Volume and tumor inhibition rate. The tumor tissues were sectioned and the expressions of Bax, Bcl-2, p-ERK1 / 2 and p-MEK1 / 2 in solid tumor tissues were detected by immunohistochemistry. Results: The average tumor weight of NGA group was significantly lower than that of tumor-bearing control group (1.29 ± 0.24), (0.21 ± 0.07), (0.41 ± 0.17) and (1.00 ± 0.28) g , The inhibition rate of high dose NGA group was 83.75%, which was higher than that of positive control 5-FU (46.54%) (P <0.05); the expression of Bax increased in a dose-dependent manner, the expression of Bcl- The expression of p-ERK1 / 2 and p-MEK1 / 2 in NGA-treated group was significantly lower than that in tumor-bearing control group (P <0.05). CONCLUSION: NGA has the exact antitumor activity against Hep G2-xenografted nude mice in vivo, and its mechanism of action and up-regulation of Bax / Bcl-2 ratio induce the apoptosis of solid tumor cells and down-regulate mitogen-activated protein kinase kinase, MAPK) signal transduction pathway phosphorylation level is closely related.