中文摘要：

目的通过观察用药后COX-2、Bcl-2和Survivin的变化，探讨丹皮酚（paeonol，Pae）诱导Eca-109食管癌裸鼠移植瘤凋亡的机制。方法体外培养食管癌Eca-109细胞。裸鼠皮下接种Eca-109细胞建立裸鼠移植瘤动物模型，36只荷瘤裸鼠随机分为6组，分别为模型对照组、Pae不同剂量组（25、50、100、200mg·kg^-1）和阳性药对照组（cisplatin，CD-DP，5mg·kg^-1）。治疗2wk后处死裸鼠，剥取瘤体称瘤重并计算抑瘤率。用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法检测肿瘤细胞凋亡。免疫组化S—P法检测移植瘤组织COX-2、Bcl-2和Survivin的表达。结果Pae50、100和200mg·kg^-1组和CDDP5mg·kg^-1组均能明显抑制裸鼠皮下肿瘤的生长，抑瘤率分别为23．54％、27．91％、34．46％和58．71％，与模型组比较差异均有显著性（P〈0．05orP〈0．01）。TUNEL染色可发现棕褐色的凋亡细胞呈散在或片状分布，Pae各剂量组的凋亡指数（apoptosisindex，AI）分别为（11．02±2．58）％、（19．80±2．77）％、（24．48±4．35）％和（27．13±4．39）％，与模型组（4．81±0．83）％比较，差异均有显著性（P〈0．05orP〈0．01）。免疫组化结果显示。Pae能明显抑制移植瘤组织COX-2、Bel-2和Survivin的表达（P〈0．05orP〈0．01）。结论Pae能抑制Eea-109食管癌裸鼠移植瘤生长、诱导凋亡而发挥抗肿瘤作用，其机制可能与下调COX-2的表达并抑制Bel-2和Survivin的表达有关。

英文摘要：

Aim To investigate the mechanism of apoptosis on human esophageal cancer Eca-109 cell carcinoma xenograft in nude mice induced by paeonol （Pae） by detecting changes of expressions of COX-2, Bcl-2 and Survivin. Methods Human esophageal carcinoma Eca-109 cells were nude mice model of the cultured in vitro. After the subcutaneous transplanting tumor was established by human esophageal cancer Eca-109 ,the nude mice were randomly divided into six groups ： various dosages of Pae treated groups （ 25,50, 100,200 mg· kg^- 1 ）, cisplatin （CDDP） positive control group （5 mg· kg^- 1 ） and model group. After two weeks of treatment, mice were killed and the tumors were taken out to weigh. The tumor inhibitory rate was calculated. Cell apoptosis in situ was examined by a TUNEL assay in the samples of carcinoma. Immunohistochemistry （S-P）was used to examine the expressions of COX-2, Bcl-2 and Survivin. Results The growth of implanted tumor was markedly inhibited in Pae groups （50,100,200 mg· kg^- 1 ） and CDDP group（5 mg· kg^- 1 ）, the inhibitory rate being 23.54%, 27.91%, 34.46%,58.71% respectively （P 〈 0.05 or P 〈 0. 01 ）. It was found that the apoptotie cells which stained yellow distributed seatterly or diffusely by TUNEL techniques. The apoptosis indexes of Pae groups were （ 11.02 ± 2. 58 ） % , （ 19. 80 ± 2. 77 ） %, （24. 48 ±4. 35）% and（27.13 ±4. 39）% respective- ly, which were significantly higher than （4. 81 ± 0. 83）% in control group（P 〈0. 05 or P 〈0. 01 ）. The expressions of COX-2, Bel-2 and Survivin in Pae groups were significantly lower than those of the control group detected by immunohistoehemistry （P 〈 0. 05 or P 〈 0. 01 ）. Conclusion Pae could inhibit the tumor growth and induce apoptosis of human esophageal carcinoma Eea-109 in vivo, the mechanism of which might be related with down-regulation of COX-2, Bel-2 and Suvivin.