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目的通过结晶硫化镍在支气管上皮细胞(16HBE)中磷酸化细胞外信号调节蛋白(P-ERK1)的表达,探讨镍致癌的分子机制。方法用SDS聚丙烯酰胺凝胶电泳和蛋白免疫印迹杂交(W estern b lot)法检测16HBE细胞中P-ERK1的表达。结果硫化镍不能明显激活P-ERK1的表达,染镍组与对照组比较差异无统计学意义(P>0.05)。结论镍不能激活P-ERK1的表达,其机制尚不清楚,硫化镍有可能激活P38和JNK通路,从而直接或间接发挥致癌作用。
Objective To investigate the molecular mechanism of nickel-induced carcinogenesis by crystallizing nickel sulfide in the bronchial epithelial cells (16HBE) to phosphorylate extracellular signal-regulated protein (P-ERK1) expression. Methods The expression of P-ERK1 in 16HBE cells was detected by SDS polyacrylamide gel electrophoresis and Western blotting. RESULTS: Nickel sulphide did not significantly activate the expression of P-ERK1, and there was no significant difference between the nickel-stained group and the control group (P>0.05). Conclusion Nickel can not activate the expression of P-ERK1. The mechanism is still unclear. Nickel sulfide may activate P38 and JNK pathways, which directly or indirectly exert carcinogenesis.