As_2O_3诱导胃癌细胞凋亡时蛋白激酶C及cAMP水平的变化

CHANGES OF cAMP AND PKC IN As_2O_3 INDUCED APOPTOSIS IN GASTIC CELLS

目的从第二信使角度探讨As2 O3 诱导胃癌BGC 82 3细胞凋亡的作用机制。方法采用免疫组化、流式细胞术 ,观察As2 O3 诱导胃癌细胞凋亡的形态学改变及凋亡率 ;采用放免方法检测As2 O3 诱导胃癌细胞凋亡时环磷酸腺苷、蛋白激酶C水平变化。结果As2 O3 能够显著增加细胞凋亡率 (P <0 .0 5 ) ,诱导细胞出现凋亡形态学改变 ;并上调胃癌细胞内环磷酸腺苷水平 (P <0 .0 1) ,下调蛋白激酶C的水平 (P <0 .0 5 )。结论As2 O3 通过上调环磷酸腺苷水平 ,下调蛋白激酶C水平诱导胃癌细胞凋亡 ,抑制细胞增殖。

ObjectiveTo illustrate changes of cAMP and protein kinase C(PKC) in arsenic trioxid (As 2O 3) induced apoptosis in gastric cancer cells.MethodsCellular morphologic changes of BGC 823 cells was observed with immunohistochemistric way. Apoptosis rate was detected by flow cytometry. Radioimmunoassay was used to detect cAMP and PKC. ResultsApoptosis rate induced by As 2O 3 was higher than control (P< 0.05 ). The level of cAMP increased (P< 0.01 ), and that of PKC decreased (P< 0.05 ) in As_2O_3-treated cells. Gastric cancer cells presented morphologic features of apoptosis.ConclusionAs_2O_3 induced BGC-823 cells apoptosis by up-reglating cAMP and down-regulating PKC.