摘要
目的:观察癌痛平胶囊对H22荷瘤小鼠肿瘤生长转移的抑制作用,探讨其作用机制。方法:ICR小鼠接种H22肝癌细胞株,建立H22荷瘤小鼠模型。将H22荷瘤小鼠随机分为模型组、顺铂组、癌痛平高、低剂量组,模型组每日ig等容积生理盐水,癌痛平高、低剂量组每日ig癌痛平(36,18 g·kg^(-1)),顺铂组每日ip顺铂(2 mg·kg^(-1))。各组连续给药7 d,处死荷瘤小鼠,剥离瘤体称重,按公式计算抑瘤率。采用免疫组化检测肿瘤组织中血管内皮生长因子(VEGF)蛋白表达,使用实时荧光定量PCR(Real-time PCR)以及免疫印迹法(Western blot)检测肿瘤组织中C-X-C趋化因子配体12(CXCL12)及C-X-C趋化因子受体4(CXCR4)基因以及蛋白表达的改变。结果:癌痛平高、低剂量显著抑制小鼠H22荷瘤小鼠肿瘤的生长,癌痛平高剂量显著降低肿瘤组织中VEGF蛋白表达,并抑制CXCL12和受体CXCR4的基因及蛋白表达(P<0.01)。结论:癌痛平胶囊对H22荷瘤小鼠肿瘤生长转移具有一定的抑制作用,其作用机制可能是通过降低肿瘤组织VEGF蛋白表达以及干预CXCL12/CXCR4生物轴抑制肿瘤转移。
Objective： To observe the inhibitory effect of Aitongping capsules on tumor growth and metastasis in H22 tumor bearing mice,and explore its mechanism. Method： The ICR mice were inoculated with hepatoma cell line H22 to establish H22 tumor-bearing mice models. The H22 tumor-bearing mice were randomly divided into model group,cisplatin group,Aitongping high and low dose groups. The mice in the model group received the same volume of normal saline by ig daily,mice in Aitongping high-dose and low-dose group received36,18 g·kg^-1Aitongping by ig daily,and the mice in cisplatin group received 2 mg·kg^-1cisplatin by ip daily.All the groups received continuous administration for 7 d,and then the mice were sacrificed. The tumor was peeled off for weighing,and the tumor inhibition rate was calculated according to the formula. Protein expression of vascular endothelial growth factor（ VEGF） in tumor tissues was detected by immunohistochemistry, gene and protein expressions of C-X-C chemokine ligand 12（ CXCL12） and its receptor C-X-C chemokine receptor 4（ CXCR4） in tumor tissues by using Real-time PCR and Western blot method. Result： Aitongping high and low dose groups significantly inhibited the growth of tumors in H22 tumor-bearing mice. Aitongping high dose group significantly decreased the protein expression of VEGF in the tumor tissues,and inhibited the gene and protein expressions of CXCR4（ P〈0. 01）. Conclusion： Aitongping capsules have a certain inhibitory effect on tumor growth and metastasis in H22 tumor-bearing mice,and its mechanism may be associated with reducing protein expression of VEGF in tumor tissues and interventing CXCL12 / CXCR4 biological axis.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2016年第11期107-110,共4页
Chinese Journal of Experimental Traditional Medical Formulae
基金
国家自然科学基金项目(81373511,81403079,81573910)
江苏省自然科学基金项目(BK20131416,BK20141467)
江苏省科技支撑计划(社会发展)资助项目(BE2012763)
