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目的:观察夜香树甾体皂苷(SSCN)对HepG2肝癌移植瘤的抑制作用,并探讨其抑瘤的可能机制。方法:从夜香树叶和嫩枝用有机溶剂提取、分离并鉴定SSCN。应用人肝癌细胞株HepG2皮下接种法建立移植瘤模型,建模成功后将荷人肝癌裸鼠随机分为5组:生理盐水组0.2 mL·次-1、沙利度胺(TLD)组200 mg·kg-1和SSCN低,中,高剂量组4,6,8 mg·kg-1。隔天ip给药,在治疗期间测量皮下移植瘤的长径和短径;30 d后处死裸鼠,免疫组化法检测移植瘤中微血管密度(MVD)和血管内皮细胞生长因子(VEGF)的表达,用酶联免疫法(ELISA)法检测裸鼠血清中白细胞介素-8(IL-8)的表达。结果:SSCN低,中,高剂量ip给药对肝癌裸鼠移植瘤相对肿瘤细胞增殖率分别为对照组(100%)的48.26%,42.94%,41.57%,TLD组的相对肿瘤增殖率为42.19%。SSCN各组及TLD组的MVD,VEGF和IL-8的水平都明显低于模型组(P<0.01)。结论:夜香树叶甾体皂苷体内对BALB/c裸鼠肝癌移植瘤有一定的抑制作用,其作用机制可能通过抑制VEGF,MVD的表达以及IL-8的转录,导致肿瘤血管生成受到抑制。
OBJECTIVE: To observe the inhibitory effect of SSCN on HepG2 hepatocellular carcinoma xenografts and to explore the possible mechanism of antitumor activity. Methods: SSCN was isolated and identified from the leaves and shoots of C. sinensis using organic solvents. Human hepatocellular carcinoma cell line HepG2 was subcutaneously inoculated to establish a transplanted tumor model. After successful modeling, nude mice bearing human hepatocellular carcinoma were randomly divided into 5 groups: saline 0.2 mL · s -1 and thalidomide 200 mg · Kg-1 and SSCN low, medium and high dose groups 4,6,8 mg · kg-1. Mice were dosed on the next day, and the long and short diameters of the transplanted tumors were measured during the treatment. After 30 days, the nude mice were sacrificed and the MVD and VEGF levels in the transplanted tumor were detected by immunohistochemistry The expression of interleukin-8 (IL-8) in nude mice was detected by enzyme-linked immunosorbent assay (ELISA). Results: The proliferation rate of tumor cells in nude mice transplanted with low, medium and high doses of SSCN was 48.26%, 42.94% and 41.57% respectively compared with control group (100%). The relative tumor proliferation rate in TLD group was 42.19 %. The levels of MVD, VEGF and IL-8 in SSCN group and TLD group were significantly lower than those in model group (P <0.01). CONCLUSION: Strychnos saponin in vivo inhibits the growth of transplanted hepatocellular carcinoma in BALB / c nude mice in vivo. The possible mechanism may be that angiogenesis may be inhibited by inhibiting the expression of VEGF and MVD and the transcription of IL-8.