摘要
目的探讨五味子乙素对Aβ25-35引起的褐家鼠肾上腺嗜铬瘤细胞PC12细胞毒性的作用,并探讨其可能机制。方法 10、25、50、75、100μmol/L五味子乙素作用于PC12细胞,MTT法筛选低毒性的五味子乙素浓度,Aβ25-35诱导PC12细胞毒性损伤建立阿尔茨海默病体外模型,加入低毒性的五味子乙素,倒置显微镜下观察细胞形态变化,MTT法检测细胞活性,RT-PCR法检测PC12细胞β淀粉样前体蛋白(amyloidβ-protein precursor,APP)基因mRNA的表达水平。结果 10、25μmol/L五味子乙素单纯处理可促进PC12细胞增殖,以10μmol/L增长作用更明显,差异具有统计学意义(P<0.05),50、75、100μmol/L五味子乙素对细胞有抑制作用,抑制率>10%;给予Aβ25-35诱导后PC12细胞存活率降低为(46.4±4.9)%,APP基因表达上调(105±9.3)%;给予10μmol/L的五味子乙素处理后的Aβ25-35组,细胞存活率升高至(107±5.5)%,APP基因表达减少(66.9±7.2)%。结论 10、25μmol/L五味子乙素均可以促进PC12细胞增长,但不具有浓度依赖性;10μmol/L五味子乙素可拮抗Aβ25-35对PC12细胞的损伤作用,机制可能是通过减少APP表达而起作用。
Objective To explore the role and the probable mechanism of schisandrin B on amyloid β-protein25-35.Methods Cultivating PC12 cells with 10,25,50,75,100 μmol/L schisandrin B respectively,the MTT method was used to select the best hypotoxic concentration of schisandrin B.Then we established the in vitro model of Alzheimer＇s disease using amyloid β-protein25-35,added the above hypotoxic schisandrin B,Afterwards we observed the stereochemical structure of PC12 cells through invert microscope,detect the activity of PC12 cells in MTT method,and reverse transcription‐PCR（RT‐PCR）was utilized to observe the expression of amyloid β-protein precursor.Results The 10,25 μmol/L schisandrin B could help PC12 cells to proliferate,especially the 10 μmol/L concentration,and 10 μmol/L schisandrin B could also effectively alleviate the cell inhibition induced by the Aβ25‐35,improve the cell activity to（107±5.5）%,and decrease the high expression of APP by（66.9±7.2）%.Conclusions 10,25 μmol/L schisandrin B could both arouse the multiplication of PC12 cells,especially the 10 μmol/L.Aβ25‐35 could induce inhibition in PC12 cells and 10 μmol/L schisandrin B may relieve this damage induced by the Aβ25‐35 through APP pathway.
出处
《卒中与神经疾病》
2010年第4期212-216,共5页
Stroke and Nervous Diseases
