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目的 探讨胃泌素和胆囊收缩素 (CCK)对胆管癌细胞凋亡阈值的调节作用。方法 以白僵菌素 (40 μmol/L× 1 2h)为凋亡诱导剂 ,末端标记 (TUNEL)技术检测胃泌素 (Gastrin) 1 7或CCK 8S(1 0 - 8mol/L× 48h)预处理后QBC939胆管癌细胞诱发性凋亡指数 (AI)的变化及反义bcl 2寡核苷酸转染 (1 .32mg/L)的影响。结果 Gastrin 1 7或CCK 8S预处理使AI显著降低 ,与对照组比较 ,差异有显著性 (P <0 .0 1 ) ,同时加入Gastrin/CCK B受体拮抗剂L365 ,2 60或转染反义bcl 2寡核苷酸可逆转 ,与相应Gastrin 1 7或CCK 8S组比较 ,差异有显著性 (P <0 .0 1 )。结论 胃泌素和CCK具有提高凋亡阈值、抑制胆管癌细胞凋亡的作用 ,其机制与上调bcl 2基因表达有关
Objective To investigate the regulatory effect of gastrin and cholecystokinin (CCK) on the apoptosis threshold of cholangiocarcinoma cells. Methods Beauveria suis (40 μmol / L × 12 h) was used as an apoptosis inducer and Gastrin 17 or CCK 8S (1 0 - 8 mol / L × 48 h) was pretreated with TUNEL The change of induced apoptotic index (AI) of QBC939 cholangiocarcinoma cells after treatment and the effect of antisense bcl 2 oligodeoxynucleotide transfection (1.32 mg / L). Results Gastrin 1 7 or CCK 8S pretreatment significantly reduced AI, compared with the control group, the difference was significant (P <0.01), while Gastrin / CCK B receptor antagonist L365, 2 60 or transfection The bcl-2 oligonucleotide was reversible, with significant difference (P <0.01) compared with the corresponding Gastrin 1 7 or CCK 8S group. Conclusion Gastrin and CCK have the effect of increasing the apoptosis threshold and inhibiting the apoptosis of cholangiocarcinoma cells. The mechanism is related to the up-regulation of bcl 2 gene expression