摘要
目的探讨淫羊藿总黄酮对1-甲基-4-苯吡啶离子(MPP+)诱导的MES23.5细胞损伤的保护作用。方法 MES23.5细胞常规培养,淫羊藿总黄酮预处理24 h,再用MPP+和淫羊藿总黄酮共同处理细胞24 h,MTT法检测细胞的存活率,实时反转录聚合酶链反应(real ti me RT-PCR)观察bcl-2和bax基因的表达情况。结果 MPP+可剂量依赖性地损伤MES23.5细胞(F=18.38,P<0.001);淫羊藿总黄酮预处理可明显对抗MPP+的毒性作用(F=44.36,P<0.001);MPP+对bcl-2基因表达没有明显影响,但可明显增加bax基因的表达(F=10.92,P<0.05);淫羊藿总黄酮预处理可明显增加bcl-2基因的表达(F=15.76,P<0.01),并可逆转bax基因表达的增高(F=10.92,P<0.05)。结论淫羊藿总黄酮可明显对抗MPP+对MES23.5神经细胞的损伤,其作用机制可能与抗凋亡有关。
Objective To study the protection of total flavonoid of Herba Epimedii (TFHE) against 1 methyi-4-pheny- lpyridinium (MPP+)-induced neurotoxicity. Methods MES23.5 cells were cultured as routine and pretreated with TFHE for 24 h, and then co-treated with MPP+ and TFHE for 24 h. The survival of the cells was observed by MTT method. The real time RT PCR was used to detect the gene expressions of bcl-2 and hax. Results MPP+ damaged MES23.5 ceils as a dose-dependent manner (F=18.38,P〈0. 001). Pretreatment with TFHE could obviously against toxic action of MPP+ (F=44.36,P〈0. 001). MPP+ had no significant effect on bcl 2 gene expression, but increased the gene expression of bax (F=10.92, P'Q0.05). Pretreat- ment of TFHE increased the bci-2 gene expression (F=15.76, P〈0.01) and reversed the increase of bax gene expression (F= 10.92,P〈0. 05). Conclusion Total flavonoid of Herba Epimedii has an antagonistic action on MES23.5 cells damage induced by MPP+ , of which, the mechanism may be related to its anti apoptosis effects.
出处
《青岛大学医学院学报》
CAS
2010年第6期471-472,476,共3页
Acta Academiae Medicinae Qingdao Universitatis
基金
国家自然科学基金资助项目(30971004)
山东省自然科学基金资助项目(Y2007D49)