目的 探究脱氢卡维丁（dehydrocavidine， DHC）单药不同剂量对人肝细胞癌Huh7细胞体外增殖、迁移、侵袭能力及小鼠肝癌Hep1-6细胞体内成瘤能力的影响，同时明确DHC与索拉非尼的抗癌效果差异及联合用药的协同效应，为肝细胞癌（hepatocellular carcinoma，HCC）的治疗提供实验依据。 方法 采用0.1、0.2、0.3 mg/mL 梯度浓度DHC处理人肝癌Huh7细胞，通过CCK-8法检测细胞增殖能力，结合平板克隆、细胞划痕及Transwell实验分别评价细胞克隆形成、迁移与侵袭水平。将对数生长期Hep1-6细胞悬液皮下注射至BALB/c-nu裸鼠右侧腋窝，建立肝癌皮下移植瘤模型；待肿瘤体积生长至约30 mm3时，将移植瘤裸鼠随机分为对照组及DHC低、中、高剂量组，开展DHC单药剂量效应体内研究；在明确DHC有效作用剂量基础上，进一步设置对照组、DHC单药组、索拉非尼单药组、DHC与索拉非尼联合组，进行药物单独干预及联合药效对比实验。各组均采用隔日腹腔注射方式规律给药，实验期间定期测量肿瘤长径与短径，并计算肿瘤体积，同时持续监测裸鼠体质量变化。 结果 DHC对Huh7细胞增殖呈浓度时间依赖性抑制（P < 0.05），各浓度组划痕愈合宽度、克隆形成数、穿膜细胞数均显著低于对照组（P < 0.05）。体内的单独给药实验中，DHC各剂量组移植瘤体积显著小于对照组（P < 0.05），且呈剂量依赖性；联合用药实验中，DHC和索拉非尼组、DHC单独组、索拉非尼单独组移植瘤体积均显著小于对照组（P < 0.05）。各组裸鼠体质量差异无统计学意义（P > 0.05），无明显毒性。 结论 DHC可剂量依赖性抑制人肝癌Huh7细胞的体外恶性表型及小鼠肝癌Hep1-6细胞的体内成瘤能力。

Objective To investigate the effects of different doses of dehydrocavidine （DHC） used as a single agent on the in vitro proliferation， migration， and invasion capabilities of human hepatocellular carcinoma Huh7 cells， as well as the in vivo tumor-forming capacity of mouse hepatocellular carcinoma Hep1-6 cells. Simultaneously， to clarify the differences in anticancer efficacy between DHC and sorafenib and the synergistic effects of combination therapy， thus providing experimental evidence for the treatment of hepatocellular carcinoma （HCC）. Methods Human hepatocellular carcinoma Huh7 cells were treated with DHC at gradient concentrations of 0.1， 0.2， and 0.3 mg/mL. Cell proliferation was assessed using the CCK-8 assay. Meanwhile， cell colony formation， migration， and invasion were evaluated using plate cloning， cell scratch， and Transwell assays， respectively. A suspension of Hep1-6 cells in the logarithmic growth phase was subcutaneously injected into the right axilla of BALB/c-nu nude mice to establish a subcutaneous liver cancer xenograft model. Once the tumour volume had reached approximately 30 mm³， the nude mice bearing xenografts were randomly divided into a control group， low-dose， medium-dose， and high-dose DHC groups to conduct an in vivo dose-response study of DHC monotherapy. Once the effective dose of DHC had been determined， additional groups were established， including a control group， a DHC monotherapy group， a sorafenib monotherapy group， and a DHC-sorafenib combination group， to conduct experiments comparing the efficacy of individual drugs and combination therapy. All groups were administered the drugs regularly via intraperitoneal injection every other day. During the experiment， the major and minor axes of the tumours were periodically measured to calculate tumour volume， and changes in the body weight of the nude mice were continuously monitored. Results DHC demonstrated a concentration- and time-dependent inhibitory effect on the proliferation of Huh7 cells （P < 0.05）. In all concentration groups， the wound healing width， the number of colony-forming units， and the number of cells crossing the membrane were significantly lower compared to the control group （P < 0.05）. In the in vivo single-agent administration experiments， the tumour volumes in all DHC dose groups were significantly smaller than those in the control group （P < 0.05）， showing a dose-dependent relationship. In the combination therapy experiments， the tumour volumes in the DHC and sorafenib group， the DHC monotherapy group， and the sorafenib monotherapy group were all significantly smaller than those in the control group （P < 0.05）. There were no statistically significant differences in the body weight among the groups of nude mice （P > 0.05）， and no obvious toxicity was observed. Conclusion DHC can inhibit， in a dose-dependent manner， the in vitro malignant phenotype of human hepatocellular carcinoma Huh7 cells and the in vivo tumourigenic capacity of mouse hepatocellular carcinoma Hep1-6 cells.