利卡灵醇是从马兜铃毛竹（Aristolochia pubescens）的根和茎中提取的一种2,3-二氢苯并呋喃新木脂素。本论文主要以利卡灵醇为研究对象，探索其在抑制肿瘤细胞生长中的作用，即该化合物体外抗肿瘤活性。本研究利用现代分子生物学、细胞生物学等实验手段对其诱导结肠癌SW480细胞凋亡的分子机制进行初步探讨，为进一步研究利卡灵醇的药理学活性奠定了理论基础；同时，以肿瘤发生的分子机制为基础，探索建立用于抗肿瘤药物筛选及其机理研究的方法体系，为新药研发的临床前基础研究提供了有价值的参考资料。 根据植物中提取天然化合物有效成分的常规研究方法，特别是对肿瘤的生长抑制作用，我们首先利用MTT筛选药物的方法，比较系列化合物对结直肠癌细胞系SW480增殖活力的影响，筛选出对SW480细胞具有明显生长抑制作用的化合物利卡灵醇。接着，我们比较了利卡灵醇对另外两种结直肠癌细胞系HCT-116，Caco-2细胞及正常细胞系HEK 293细胞生长抑制的影响。结果表明，利卡灵醇能够特异性且呈剂量依赖性抑制结直肠癌 SW480细胞的增殖并诱导其发生凋亡。因此，我们以肿瘤增殖的两个关键事件细胞周期和细胞凋亡为药物筛选的靶标事件，以调控这两个核心事件的关键调控因子为分子靶标，利用体外细胞模型进一步研究利卡灵醇对SW480细胞增殖的影响及其分子机理。 通过流式细胞术，我们发现利卡灵醇能够通过调控p21、Cyclin D1及CDK2等细胞周期相关基因的表达，将SW480细胞分裂阻滞在G1/S期。同时，其还能通过影响细胞凋亡基因Caspase 3的活性，诱导SW480细胞发生凋亡。 接下来，我们对利卡灵醇影响SW480细胞生长的机制进行了研究，发现其能通过降低p-STAT3(Y705)和p-STAT3(S727)水平抑制STAT3信号通路，进而影响下游功能基因表达，最终导致SW480细胞凋亡的发生。综上，本研究表明，利卡灵醇对于SW480细胞系具有显著的体外抗肿瘤活性，能够通过抑制STAT3信号通路诱导SW480细胞发生凋亡，说明利卡灵醇有可能成为临床治疗结肠癌的潜在药物。

Licarinediol is a 2,3-Dihydrobenzofuran neolignan found in stems and roots of Aristolochia pubescens, This study focused on inhibitory effects of Licarinediol on cancer cells, that is the the antitumor activities in vitro. Based on this, modern molecular biology and cellular pharmacology were employed to study the molecular mechanisms of apoptosis effect on SW480 cell as a preliminary study to lay the theoretical foundation for further study of pharmacological activity; meanwhile, based on molecule mechanisms of tumorigenesis, established methodology to explore mechanisms for screening anticancer drugs, provide valuable reference for basic research in preclinical drug development.According to popular research of plant extract active ingredients, especially growth inhibition based on features of strong proliferation of tumor cell, we first use the drug screening methods based on MTT assay to observe series of compounds on colorectal cancer cell lines SW480 and Licarinediol has significantly inhibition. Secondly, compare inhibitory effects of Licarinediol for the other two colorectal cancer cell lines HCT-116, Caco-2 cells and normal HEK 293. We presented here that Licarinediol only inhibited proliferation and induced apoptosis of colon cancer cells, SW480, in a dose-dependent manner. Therefore, Selected cell cycle and apoptosis two key events in proliferation of tumor cells as targets for drug screening, and series of regulators as molecular targets, to further study molecular mechanisms of Licarinediol on SW480 in vitro.By PI staining-FACS analysis and Annexin V-FITC binding assay, we found that Licarinediol changed distribution of cell cycle and induced arrest in G1 / S phase; significantly enhanced apoptosis in a dose-dependent manner during apoptosis, another target event. Further studies on molecular mechanisms indicated those correlated with an increase in p21 and a decrease in cyclin D1 and CDK2, Caspase 3 apoptotic factors respectively. We also demonstrated that STAT3 signaling pathway which is important in the regulation of physiological processes, such as proliferation, differentiation and apoptosis may play a role. STAT3 activation and deactivation are strictly regulated, which are continuous activated in many tumor tissues and cell lines. Licarinediol significantly reduced p-STAT3 (Y705), and p-STAT3 (S727) levels. In addition, Licarinediol also inhibited the expression of the downstream genes of STAT3 related to cell cycle regulation and apoptosis. In general, Licarinediol has significant antitumor activity via cell cycle arrest and apoptotic induction in SW480 cells. These results suggest that Licarinediol has therapeutic potential against human colon carcinoma.