目的:探讨肿节风提取物对人鼻咽癌细胞株CNE1、CNE2裸鼠移植瘤的抑瘤作用及与瘤细胞凋亡的关系。方法:采用CNE1、CNE2细胞接种于裸鼠腋下,1周后成瘤,建立肿瘤模型,灌胃给药30 d;TUNEL法检测细胞凋亡;流式细胞仪进行细胞凋亡的分析;透射电镜观察瘤组织细胞超微结构的改变;免疫组化法检测瘤组织Bc l-2,Bax的表达。结果:肿节风治疗组的裸鼠瘤重、肿瘤相对体积明显低于对照组(P<0.01);TUNEL法检测肿节风组凋亡指数高于对照组(P<0.01);流式细胞技术显示肿节风组凋亡率分别为58.34%和63.76%,与对照组相比有统计学意义(P<0.01);电镜下用药组瘤组织中可见较多典型的细胞凋亡的形态学表现;免疫组化结果显示Bc l-2蛋白的表达明显低于对照组(P<0.01),而Bax蛋白的表达明显高于对照组(P<0.01)。结论:肿节风在体内具有抑制CNE1、CNE2移植瘤生长的作用,其机制与下调Bc l-2蛋白、上调Bax蛋白的表达进而促进肿瘤细胞的凋亡有关。 OBJECTIVE: To investigate the inhibitory effect of Tuofengye extract on human nasopharyngeal carcinoma cell lines CNE1 and CNE2 in nude mice and its relationship with tumor cell apoptosis. METHODS: CNE1 and CNE2 cells were inoculated into the axilla of nude mice. Tumors were formed one week later. A tumor model was established and administered by gastric gavage for 30 days. Apoptosis was detected by TUNEL assay; apoptosis was analyzed by flow cytometry; transmission electron microscopy was performed. The ultrastructural changes of the tumor tissue were detected; the expression of Bcl-2 and Bax in the tumor tissue was detected by immunohistochemistry. RESULTS: Tumor weight and relative volume of tumor in nude mice treated with swollen wind were significantly lower than those in the control group (P<0.01). Apoptotic index was detected by TUNEL method in the tumor group compared with the control group (P<0.01); flow cytometry The technique showed that the apoptotic rates in the Tuofengfeng group were 58.34% and 63.76%, respectively, which was statistically significant compared with the control group (P<0.01); the morphology of the tumor cells in the medication group under the electron microscope showed more typical morphology of apoptosis. Performance; Immunohistochemistry results showed that Bcl-2 protein expression was significantly lower than the control group (P <0.01), while the expression of Bax protein was significantly higher than the control group (P <0.01). CONCLUSION: Tumorous wind can inhibit the growth of CNE1 and CNE2 transplanted tumors in vivo. The mechanism is related to the down-regulation of Bcl-2 protein, up-regulation of Bax protein expression, and promotion of apoptosis of tumor cells.