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目的:观察体外培养的大鼠大脑皮质星形胶质细胞(Ast)在模拟脑缺血再灌注后分泌脑源性神经营养因子(BDNF)、胶质细胞源性神经营养因子(GDNF)、热休克蛋白70(HSP70)和白细胞介素6(IL-6)的变化以及中药抗呆Ⅰ号的影响。方法:实验于2002-03/2004-05在北京中医药大学完成。在大鼠大脑皮质Ast分离纯化培养的基础上体外模拟脑缺血再灌注,采用免疫细胞化学方法来观察受损Ast在缺血4h,再灌注3,18,24,36,48,72h后分泌BDNF,GDNF,HSP70和IL-6的动态变化及抗呆Ⅰ号的作用。结果:①体外培养的大鼠大脑皮质Ast在体外模拟脑缺血再灌注损伤后其分泌BDNF,GDNF,HSP70和IL-6的能力增强。②抗呆Ⅰ号可使受损Ast的分泌功能更加增强。结论:①体外模拟脑缺血再灌注使受损的Ast发生反应性胶质化,表现为分泌神经营养因子、炎性细胞因子及应激反应蛋白的能力增强。②抗呆Ⅰ号通过增强Ast的分泌功能来保护和修复受损的神经组织。
OBJECTIVE: To observe the secretion of brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and heat in rat cortical astrocytes cultured in vitro after simulated cerebral ischemia-reperfusion Changes of shock protein 70 (HSP70) and interleukin 6 (IL-6) and effects of traditional Chinese medicine anti-dead I. METHODS: The experiment was completed at the Beijing University of Traditional Chinese Medicine from March 2002 to May 2004. Brain ischemia and reperfusion were simulated in vitro on the basis of the isolation and purification of rat cerebral cortex Ast. Immunocytochemistry was used to observe that the damaged Ast was secreted for 4 hours after ischemia and 3, 18, 24, 36, 48, and 72 hours after reperfusion. Dynamic Changes of BDNF, GDNF, HSP70, and IL-6 and the Effect of Antidetention. RESULTS: (1) The ability of Ast to excrete BDNF, GDNF, HSP70 and IL-6 in cerebral cortex after in vitro brain injury. 2 Anti-dead I can make the secretion of damaged Ast even more enhanced. Conclusion: 1 In vitro simulated cerebral ischemia-reperfusion induced reactive gelatinization of damaged Ast, which showed enhanced ability to secrete neurotrophic factors, inflammatory cytokines and stress response proteins. 2 Kangdai I protects and repairs damaged nerve tissue by enhancing the secretory function of Ast.