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目的 研究极低频 (ELF)磁场抑制细胞间隙连接通讯 (GJIC)的分子机制。方法 NIH3T3小鼠成纤维细胞受 5 0Hz、0 .8mTELF(2 4h)、12 氧 14 酰佛波 13酯 (TPA ,2h)或ELF加TPA的作用后 ,用Northern和Western印迹法检测连接蛋白 (Cx43)的基因转录水平及其磷酸化状态。结果 各处理组的Cx43基因转录水平与对照组比较 ,差异无显著性 (P >0 .0 5 )。Cx43的非磷酸化条带在正常组为 10 7.33± 2 7.42 (以样本Cx43基因条带的特异吸光度值与相对应的GAPDH吸光度值之比来表示 ) ,与ELF处理组 (6 4.6 9± 2 7.88)、TPA处理组 (45 .5 4± 2 0 .5 9)和ELF +TPA处理组 (39.96±11.93)比较 ,差异有显著或极显著性 (P <0 .0 5、P <0 .0 1) ,在各处理组间则差异无显著性 (P >0 .0 5 )。各处理组均出现了过磷酸化的P3 条带。结论 ELF和 (或 )TPA不影响Cx43基因的转录 ;ELF和 (或 )TPA抑制GJIC的主要机制是Cx43蛋白的过磷酸化。
Objective To study the molecular mechanism of the inhibition of cell gap junctional communication (GJIC) by ELF magnetic fields. METHODS: NIH3T3 mouse fibroblasts were exposed to 50 Hz, 0.8 M TEF (24 h), 12 Oxytetraspluconate 13 (TPA, 2 h) or ELF plus TPA. Connexins were detected by Northern and Western blotting. Cx43) gene transcription levels and their phosphorylation status. Results Compared with the control group, the transcription level of Cx43 gene in each treatment group was not statistically significant (P > 0.05). The non-phosphorylated band of Cx43 in the normal group was 10 7.33±2 7.42 (expressed as the ratio of the specific absorbance value of the sample Cx43 gene band to the corresponding GAPDH absorbance value), and the ELF treated group (6 4.6 9±2) 7.88), TPA treatment group (45.54 ± 20.59) and ELF + TPA treatment group (39.96 ± 11.93), the difference was significant or extremely significant (P <0.05, P <0. 0 1) , there was no significant difference between treatment groups (P > 0.05). Hyperphosphorylated P3 bands appeared in each treatment group. Conclusion ELF and (or) TPA do not affect the transcription of Cx43 gene; the main mechanism of ELF and/or TPA in inhibiting GJIC is the hyperphosphorylation of Cx43 protein.