摘要
目的探讨中药提取单体芹黄素对体外原代培养条件下Aβ2535诱导的海马神经元损伤的影响。方法采用SD大鼠海马神经元原代培养,经终浓度分别为5、10、20、40、80μmol·L-1的芹黄素预处理后,用10μmol·L-1的Aβ2535处理24h,MTT法比较神经元的存活情况、Hochesst荧光染色检测神经元的凋亡,并测定SOD活性及Bclxl蛋白表达的变化。结果芹黄素10、20、40μmol·L-1组可提高海马神经元存活率和引起Bclxl蛋白表达的增加,增加MnSOD活性、促进Cu与聚集型Aβ2535结合,而且10、20μmol·L-1芹黄素剂量组与雌二醇抗Aβ2535毒性损伤效果相同(P>0.05)。结论芹黄素对Aβ2535的毒性损伤的海马神经元具有保护作用,其保护作用可能与提高Bclxl蛋白表达、增加MnSOD活性、促进Cu与聚集型Aβ2535结合,使之转变成无毒性的可溶状态有关。
Aim To explore the ettects ot apigenin on Aβ25-35 induced injury in primary cultured hippocampal neurons. Methods The primary cultured hippocampal neurons were exposed to 10 μmol ·L^-1 Aβ25-35 for 24 h after pretreatment with the apigenin of concentrations of 5,10,20,40 μmol ·L^-1 for 2 h;then the survival rate of hippocampal and SOD activity were examined;we also analysed the expression of apoptosis-related gene bcl-xl with Western blot. Result The survival rate of hippocampal neurons were decreased after pretreatment with 10 and 20 μmol ·L^-1 apigenin for 2 h,the increases of Mn-SOD activity and bcl-xl protein expression were also observed. Conclusion Apigenin has the bioactivity of protecting the neuron from cytoxic induced by Aβ25-35 in cultured hipocampal neurons as estrogen. The mechanism is likely related with activating the SOD and increasing bcl-xl protein expression ,which plays a pivotal role in protecting cells from apoptosis.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第8期996-998,共3页
Chinese Pharmacological Bulletin
基金
广东省自然科学基金资助项目(No010086)
