CAJ | 학술논문

目的：研究表没食子儿茶素没食子酸酯（EGCG）与西妥昔单抗联用体内外抗食管癌 Eca-109的作用。方法采用 MTT法检测化合物对肿瘤细胞增殖的影响；采用克隆形成法检测 EGCG对肿瘤细胞克隆形成的影响；采用流式细胞术检测化合物对肿瘤细胞凋亡的影响；采用动物实验评价药物或 EGCG对移植于裸鼠的移植瘤的生长抑制作用；同时采用免疫组化的方法检测药物或 EGCG对血管形成的影响。结果 EGCG能够剂量依赖性地抑制 Eca-109细胞增殖，其 IC50值为43.22μmol/L。经克隆形成法检测结果表明， EGCG能够明显抑制 Eca-109细胞的克隆形成，IC50值为28.49μmol/L。EGCG能够显著引起 Eca-109细胞凋亡，60和80μmol/L EGCG诱导的凋亡百分率分别为（21.70±0.62）%、（57.13±9.09）%。EGCG和西妥昔单抗联用对 Eca-109细胞的增殖抑制作用较单独用药组强，具有相加作用。体内实验结果表明， EGCG 和西妥昔单抗均能抑制 Eca-109裸鼠移植瘤的生长，两者联用存在增强作用。EGCG和西妥昔单抗均能抑制裸鼠移植瘤的血管形成，两者联用血管形成抑制作用较单用组更强。结论 EGCG能够抑制食管癌 Eca-109的细胞增殖和克隆形成，具有诱导 Eca-109细胞凋亡作用，与西妥昔单抗联用在体内外均具有增强作用。
목적：연구표몰식자인다소몰식자산지（EGCG）여서타석단항련용체내외항식관암 Eca-109적작용。방법채용 MTT법검측화합물대종류세포증식적영향；채용극륭형성법검측 EGCG대종류세포극륭형성적영향；채용류식세포술검측화합물대종류세포조망적영향；채용동물실험평개약물혹 EGCG대이식우라서적이식류적생장억제작용；동시채용면역조화적방법검측약물혹 EGCG대혈관형성적영향。결과 EGCG능구제량의뢰성지억제 Eca-109세포증식，기 IC50치위43.22μmol/L。경극륭형성법검측결과표명， EGCG능구명현억제 Eca-109세포적극륭형성，IC50치위28.49μmol/L。EGCG능구현저인기 Eca-109세포조망，60화80μmol/L EGCG유도적조망백분솔분별위（21.70±0.62）%、（57.13±9.09）%。EGCG화서타석단항련용대 Eca-109세포적증식억제작용교단독용약조강，구유상가작용。체내실험결과표명， EGCG 화서타석단항균능억제 Eca-109라서이식류적생장，량자련용존재증강작용。EGCG화서타석단항균능억제라서이식류적혈관형성，량자련용혈관형성억제작용교단용조경강。결론 EGCG능구억제식관암 Eca-109적세포증식화극륭형성，구유유도 Eca-109세포조망작용，여서타석단항련용재체내외균구유증강작용。
Objective To explore the antitumor effect of the combination of EGCG and cetuximab on human esophageal cancer cell line Eca-109in vitro andin vivo. Methods MTT assay and colony formation assay were used to detect the effect of cell proliferation. Cellular apoptosis was examined using flow cytometry. Animal experiments were performed to evaluate the reduced growth of tumor xenograft in nude mice administrated by EGCG and cetuximab. Immunohistochemical technique was applied to examine the expression of endothelial cells in tumor tissue. Results EGCG inhibited the proliferation of Eca-109 cells in a dose-dependent manner and the IC50 value was 43.22μmol/L. The results from colony formation assay showed that EGCG dose-dependently decreased the number of colony formation at the IC50 value of 28.49μmol/L. EGCG also induced apoptosis of Eca-109 cells and the percentage of apoptosis was (21.70 ± 0.62)% and (57.13 ± 9.09)% at the concentration of 60 and 80μmol/L, respectively. The inhibitory effect of the combination of EGCG and cetuximab on the proliferation was more potent than that of either single treatment with EGCG or cetuximab, indicating an additive effect for the combination treatment. At the same time, the combination reduced the growth of tumor xenografts in nude mice more potently than EGCG or cetuximab alone. Moreover, expression level of CD31 in the tumor tissue from xenografts in the combination group was decreased more significantly than that of single EGCG or cetuximab treatment. Conclusion EGCG inhibits the proliferation and colony formation, and induces significantly apoptosis in human esophageal cancer cell line Eca-109. An additive effect was observed for the combination of EGCG and cetuximab treatment on the growth of Eca-109 cellsin vitro andin vivo.