【摘要】 目的探讨白藜芦醇对Aβ25-35诱导PC12细胞损伤的保护作用。方法用不同浓度的Aβ25-35处理PC12细胞,建立细胞毁损模型,然后加入不同浓度的白藜芦醇,在显微镜下观察PC12细胞形态的变化及突起生长情况。采用MTT检测技术观察PC12细胞的生长活性,采用酶标仪检测乳酸脱氢酶(LDH)的活性,采用瑞士-吉姆萨染色和流式细胞术检测细胞凋亡情况。结果损伤组加入Aβ25-35,24 h后细胞形态不规整,突起出现不同程度的肿胀破裂,48 h后见不到完整的突起结构;保护组加入白藜芦醇预孵育后明显延缓突起损伤,24 h后仍能观察到比较完整的突起结构,48 h后远端发生轻微断裂。保护组细胞突起长度和D(λ)值明显大于损伤组(P<0.01),细胞凋亡数以及LDH活性明显低于损伤组(P<0.01)。结论白藜芦醇对Aβ25-35诱导的PC12细胞损伤具有明显的保护作用。更多还原

【Abstract】 Objective To explore the protective effect of resveratrol on Aβ25-35-induced injury in PC12 cells.Methods PC12 cells were treated with Aβ25-35 of different concentrations to establish the Alzheimer’s disease models.Resveratrol of different concentrations were added into culture medium to detect the protection.The changes of cell morphology and neurite outgrowth were observed under a microscope.Cell activity was identified by MTT analysis.Lactate dehydrogenase(LDH) activity was identified by ELIASA.Cell apoptosis was detected by Giemsa staining and annexinV-FITC/PI double staining flow cytometry.Results PC12 cells treated with Aβ25-35 suffered axonal degeneration in the distal end of the axons at 24 h.The axons were disrupted at 48 h.The protection group with the pre-incubation of resveratrol significantly delayed axonal injury.The axons remained relatively good structures at 24 h,and the axons only suffered minor fractures at 48 h.The axon length and D(λ)value of the protection group were significantly larger than those of the injury group(P<0.01).The apoptosis and LDH activity of the protection group were significantly lower than those of the injury group(P<0.01).Conclusion Resveratrol plays an important role in protecting Aβ25-35-induced injury in PC12 cells.更多还原