雷公藤内酯醇对AD细胞模型炎性因子的影响

目的]以Aβ1-42寡聚体为工具药建立AD细胞模型,观察雷公藤内酯醇（T10）对AD的防治作用并初步探讨其作用机制。方法]用不同浓度的T10（10-11、10-10、10-9、10-8mol/L）预孵育小胶质细胞12h,然后加入10μmol/LAβ1-42共孵育12h,ELISA法检测上清TNF-α、IL-1β的含量,收获条件培养基,加入海马神经元中,作用24h,MTT法检测神经元存活率。结果]在体外T10可减少Aβ1-42诱导的小胶质细胞TNF-α、IL-1β的释放,提高海马神经元的存活率。结论]T10可通过抑制小胶质细胞激活保护海马神经元。

Effects of Triptolide on Inflammatory Factors in Alzheimer's Disease Cell Model

Objective]To observe the preventive and therapeutic effects of T10 and its mechanism on Aβ1-42 oligomer mediated Alzheimer's Disease(AD) .Method]The microglia cells were pre-treated with 10-11-10-8 M T10 for 12h before 10 μM Aβ1-42 were added,and incubated for 12 hours together.The content of TNF-α and IL-1β in supernatant was determined by ELISA .The conditioned medium was collected and was added with the hippocampus neurons for 24 hours.The survival rate of the neurons was detected by MTT.Result]T10 could significantly decrease the release of TNF-α and IL-1β induced by Aβ1-42 from microglia in vitro and raise the survival rate of the hippocampus neurons.Conclusion]T10 could protect the hippocampus neurons through inhibiting the activation of microglia.