摘要
目的 :研究调心方和补肾方对Aβ 1 42所致神经毒模型海马神经元存活率和突触小泡蛋白表达的影响。 方法 :原代培养大鼠海马神经元 ,用 2 5 μmol/L聚集状态的Aβ 1 42建立神经细胞毒模型。采用FDA与PI双染后细胞计数、LDH释放量来检测神经元存活率 ,应用免疫细胞化学法研究突触小泡蛋白的蛋白表达。结果 :神经元经Aβ 1 42处理后 ,活细胞数减少 ,LDH释放增加 ,突触小泡蛋白表达减少。调心方、补肾方使活细胞数提高 ,LDH释放减少 ,突触小泡蛋白表达回升。Tacrine使神经元存活率增加 ,但突触小泡蛋白表达的变化不明显。结论 :调心方与补肾方对Aβ 1 42神经细胞毒有保护作用 ,可提高细胞存活率 ,使突触小泡蛋白表达回升 ,但两方作用无显著差异。Tacrine对神经元存活率有提高作用 。
Objective:To study the effect of XB and ST Recipes (XBR and STR) on the neuronal survival and synaptophysin expression of hippocampal neurons in β-amyloid induced neurotoxic model. Methods: In order to establish neurotoxic model, the primary cultured rat hippocampal neurons were treated with 25μmol/L aggregated β-amyloid fragment l-42 (Aβ1-42). Neuronal survival was assessed by viable counting after double-stained with fluorescein diacetate (FDA) and propidium iodide (PI) as well as lactate dehydrogenase (LDH) activity. The protein expression of synaptophysin were examined by using immunocytochemical SABC method. Results: In the Aβ treated neurons, the number of viable cell decreased, whereas release of LDH increased. The immunoreactivity of synaptophysin was reduced. After giving XBR or STR treatment, the number of viable cell was increased, while release of LDH was decreased. The immunoreactivity of synaptophysin was strengthened. Conclusions: XBR and STR could attenuate the neurotoxic action of Aβ and improve neuronal survival, make synaptophysin expression up-regulation. XBR and STR had no significant difference in improving neuronal survival and elevating synaptophysin expression. Tacrine could improve neuronal survival, but its regulating on synaptophysin expression was not significant.
出处
《中药药理与临床》
CAS
CSCD
2000年第6期27-29,共3页
Pharmacology and Clinics of Chinese Materia Medica
基金
国家自然科学基金重点项目! (NO .39830 4 50 )
上海市教委科技发展基金!(NO 98CJ0 1 )
