摘要
目的研究抗抑郁药万拉法辛对β淀粉样蛋白片段(Aβ25-35)诱发PC12细胞损伤的保护作用。方法将培养的PC12细胞分为3组:正常对照组、Aβ损伤组和药物保护组。Aβ损伤组用Aβ25-35处理细胞,药物保护组在用Aβ25-35处理前2h加入抗抑郁药万拉法辛。采用细胞形态学方法、LDH法、MTT法、免疫组化法及western blot法观察抗抑郁药万拉法辛的保护作用。结果药物保护组与Aβ损伤组相比细胞数显著增多,受损变圆的细胞数较少;LDH释放量较少(P<0.01);OD490值显著升高(P<0.01)。Aβ损伤组中Bcl-2的表达比正常对照组低,药物保护组Bcl-2的表达比Aβ25-35损伤组升高;药物保护组、Aβ损伤组与对照组相比细胞内Bax蛋白表达均无明显变化。结论抗抑郁药万拉法辛对Aβ25-35诱发PC12细胞损伤有保护作用,其机制可能和万拉法辛升高Bcl-2蛋白水平有关。
Objective To study the protective effects of venlafaxine on injury of pheochromocytoma （PC12）
cells induced by β-amyloid peptide （Aβ）. Methods Culturing cells in medium with Aβ25-35. Venlafaxine was added in the medium. Morphological observation ,MTT assays ,I.DH assays were used to study the protective effects of venlafaxine. The level of Bcl-2 in PC12 cells was detected by using Western blot method. The expression of Bax was analyzed by using immunohistochemical technique. Results Venlafáxine attenuated round shaped cells induced by Aβ,increased OD490,decreased LDH release from PC12 and increased the level of Bcl-2,but the expression of Bax was no differences among protective group, normal control group and group. Conclusion Venlafaxine prevent PC12 cells from injury by Aβ25-35 and the mechnism may be related to the increase of the level of Bcl-2.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2007年第4期406-408,共3页
Journal of Apoplexy and Nervous Diseases
