COX-2抑制剂抑制小鼠胃癌NF-κB激活的实验观察

COX-2 Inhibitors Suppress Activation of NF-κB in Gastric Cancer

目的观察非甾体消炎药在动物体内抑制胃癌NF-κB激活的效应,探讨其抗癌机制。方法建立人胃癌细胞SGC7901裸鼠种植瘤模型,随机分为3组:舒林酸组(8 mg)、塞来昔布组(10 mg)和对照组(阿拉伯树胶50mg);采用ELISA法检测活性NFκ-B水平。结果舒林酸组(0.46±0.31)和塞来昔布组(0.23±0.08)活性NF-κB水平较对照组(0.84±0.58)明显下降(F分别为3.98、3.65,P均<0.05),舒林酸组与塞来昔布组之间差异无显著性(P>0.05)。结论非甾体消炎药在体内具有显著抗胃癌效应,抑制NFκ-B激活可能是其发挥抗癌的机制之一。

Objective To observe the inhibitory effects in vivo of nonsteroidal antiinflammatory drugs （NSAIDs） on activation of NF-κB in gastric cancer of animal model, further to investigate their anti-cancer mechanisms. Methods Thirty athymic mice＇s xenograft models with human gastric cancer cell SGC7901 were established and divided randomly into three groups, sulindac group （8 mg）, celecoxib group （10 mg）, and control group （Arabic gel 50 mg）. TransAM NFκB p50 Transcription Factor Assay Kit was applied to detect the level of activating NF-κB. Results Sulindac and celecoxib both markedly depressed the activation of NF-κB. The ANOVA analysis showed the activating NF-κB levels of both sulindac and celecoxib groups （0.46± 0.31, 0.23±0.08, respectively） were significantly lower than that of control group （0.84±0. 58,F = 3.98 and F = 3.65,P〈0.05 in both）, but no differences of activating NF-κB level showed between two drug groups. Conclusion The NSAIDs had obvious anti-cancer effects in vivo against gastric cancer, and inhibiting the activation of NF-κB might be one of their anti-cancer mechanisms.