摘要
目的:通过OGD/R处理PC12细胞,证明NaAc在人类缺血性脑卒中中的作用和意义。方法:OGD模型的建立:用无氧糖培养液处理PC12细胞作为脑缺血再灌注损伤的体外模型;使用CCK-8比色法检测OGD损伤后NaAc对PC12细胞的保护状况;使用免疫印迹法Western blot检测OGD损伤后的NaAc对PC12中ATF-6蛋白水平的影响。结果:OGD损伤后,补充浓度为6 mM的NaAc可增加PC12的存活率(n = 6, F = 70.10, P < 0.05);OGD损伤后,PC12中ATF-6的表达升高(t = 2.98, P < 0.05);向正常的PC12细胞补充NaAc后ATF-6表达降低(t = 3.11, P < 0.05);在损伤后的PC12细胞中添加浓度为6 mM的NaAc后,ATF-6的表达水平降低(n = 6, F = 2.09, P < 0.05)。结论:OGD损伤后,PC12中添加浓度为6 mM的NaAc是通过抑制ATF-6的表达来发挥神经保护作用。
Objective: The purpose of investigating is demonstrated the effect and significance of NaAc in hu-man ischemic stroke by OGD/R treatment of PC12 cells. Methods: Establishment of OGD model: treatment of PC12 cells with Anaerobic sugar culture solution culture solution as an in vitro model of cerebral ischemia reperfusion injury;The protective status of NaAc on PC12 cells after OGD injury was detected using CCK-8 colorimetry;Effects of NaAc after OGD injury on ATF-6 protein levels in PC12 were detected using Western blotting methods. Results: After OGD injury, NaAc 6 mM sup-plementation increased PC12 survival (n = 6, F = 70.10, P < 0.05) and increased ATF-6 expression in PC12 (t = 2.98, P < 0.05). Supplementation of NaAc 6 mM to normal PC12 reduced the expression of ATF-6 (t = 3.11, P < 0.05). On the contrary, after OGD Supplementation of NaAc 6 mM to PC12 re-duced the expression of ATF-6 (n = 6, F = 20.09, P < 0.05). Conclusion: After OGD injury, intra-PC12 NaAc 6 mM supplementation exerts neuroprotective effects by inhibiting the expression of ATF-6 signaling pathway.
出处
《临床医学进展》
2022年第10期9582-9588,共7页
Advances in Clinical Medicine
