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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 investigate the effect of Schisandrin B on the cytotoxicity of PC12 cells induced by Aβ25-35 in adrenal chromaffin cells of Brown Rat and to explore its possible mechanism. Methods Ten, 25, 50, 75 and 100μmol / L Schisandrin B were used to treat PC12 cells. MTT assay was used to screen low concentration of Schisandrin B and Aβ25-35 induced PC12 cell injury. The in vitro model of Alzheimer’s disease was established. The cytotoxicity of Schisandrin B was observed under an inverted microscope. The cell viability was measured by MTT assay. The mRNA expression of amyloid β-protein precursor (APP) gene in PC12 cells was detected by RT-PCR. Results Treatment with 10,25μmol / L Schisandrin B could promote the proliferation of PC12 cells, and the effect of 10μmol / L was more obvious (P <0.05). Schisandrin B at 50, 75 and 100μmol / (46.4 ± 4.9)%, and the expression of APP was up-regulated (105 ± 9.3)%. After treated with 10μmol / L Schisandrin B, the survival rate of PC12 cells was decreased Aβ25-35 group, the cell survival rate increased to (107 ± 5.5)%, APP gene expression decreased (66.9 ± 7.2)%. Conclusions Both 10 and 25μmol / L Schisandrin B can promote the growth of PC12 cells but not in a concentration-dependent manner. 10μmol / L Schizandrin B can antagonize the injury of PC12 cells by Aβ25-35, which may be caused by the decrease of APP expression effect.