[摘 要] 目的：探讨紫草素（SK）联合肿瘤细胞裂解物（TCL）刺激的DC疫苗的抗肿瘤效果。方法：体外制备SK和TCL刺激的正常小鼠源的DC疫苗，流式细胞术检测DC表面CD80、CD86的荧光强度。流式细胞术检测与SK + TCL刺激的DC共培养后的正常小鼠脾T细胞中T-bet和RORγt的表达，ELISA检测共培养上清液中IFN-γ、IL-12P70和TNF-α的含量。建立Lewis肺癌3LL细胞荷瘤小鼠模型，分为PBS（1 mL）+ TCL（5 × 105个细胞/100 μL）、SK-L（1.25 mg/kg） + TCL、SK-M（2.5 mg/kg） + TCL、SK-H（5 mg/kg） + TCL、紫杉醇（PTX 2 mg/kg） + TCL疫苗组。疫苗接种结束后10 d，检测移植瘤体积和小鼠生存率，LDH法检测脾CTL的杀伤能力。结果：SK + TCL刺激的DC疫苗表达出高水平CD80、CD86（均P < 0.01）；DC与T细胞共培养液上清中IL-12P70、IFN-γ、TNF-α含量均显著上升（均P < 0.01），T细胞中T-bet和RORγt的表达显著性上调（均P < 0.01）。成功构建Lewis肺癌荷瘤小鼠模型，SK-H + TCL刺激的DC疫苗治疗显著延缓了的移植瘤生长并提高了小鼠的存活率，且可强烈诱导脾CTL的杀伤能力（均P < 0.01）。结论：SK + TCL刺激的DC疫苗可激活DC至成熟状态，上调T细胞中T-bet和RORγt的表达，启动Th1效应细胞，SK体内治疗Lewis肺癌荷瘤小鼠具有良好的抗肿瘤效果。

With the development of genetics and molecular biology, the research on acute intermittent porphyria (AIP) has been gradually deepened, and its complication hepatocellular carcinoma (HCC) has attracted more and more attention. This article mainly summarizes the research advances in the pathogenesis and prevention of HCC in AIP. The pathogenesis of AIP with HCC is associated with oxidative stress, p53 mutation, downregulation of Bcl-2, increase in inflammatory cytokines, and iron overload, and its prevention strategies include the use of statins, strict management, liver transplantation, gene therapy, and enzyme replacement therapy. This article reviews the latest advances in the pathogenesis and prevention of AIP with HCC.