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目的研究缺氧对PC12细胞HIF-1/JAK2/NF-κB信号级联的影响。方法制备缺氧细胞模型,采用EMSA、半定量RT-PCR技术和Western blot法检测JAK2、HIF-1α、HIF-1β基因mRNA和蛋白表达水平以及NF-κB活性。结果PC12细胞JAK2、HIF-1α、HIF-1βmRNA和蛋白在缺氧后表达增强,6h达到高峰,显著高于正常对照组;PC12细胞核内NF-κB活性在缺氧后6h达到高峰,12h下降。加入JAK2抑制剂AG490后缺氧6h NF-κB活性明显降低。结论缺氧能增强JAK2、HIF-1α、HIF-1β的表达。HIF-1能激活JAK2,对缺氧受损脑组织有保护作用。
Objective To investigate the effect of hypoxia on the signal cascades of HIF-1 / JAK2 / NF-κB in PC12 cells. Methods The hypoxic cell model was established. The mRNA and protein expression of JAK2, HIF-1α and HIF-1β and the activity of NF-κB were detected by EMSA, semi-quantitative RT-PCR and Western blot. Results The expression of JAK2, HIF-1α, HIF-1βmRNA and protein in PC12 cells increased after hypoxia and peaked at 6h, which was significantly higher than that in normal control group. The activity of NF-κB in PC12 cells peaked at 6h and decreased at 12h. After adding JAK2 inhibitor AG490, the activity of NF-κB in hypoxia 6h significantly decreased. Conclusion Hypoxia can enhance the expression of JAK2, HIF-1α and HIF-1β. HIF-1 activates JAK2, which has protective effects on hypoxic damaged brain tissue.