摘要
目的:探讨Aβ25-35(β-amyloid)诱导PC12细胞凋亡过程中氯通道阻断剂Phloretin的保护作用及其机制.方法:采用MTT比色,LDH(lactate dehydrogenase)活力检测、Hoechst33258染色和琼脂糖凝胶电泳比较正常对照组、Aβ25-35损伤组和Aβ25-35+Phloretin组的PC12细胞存活与凋亡;Western Blot印迹检测3组的JNK,P-JNK蛋白表达.结果:10 mmol/L Phloretin可明显抑制Aβ25-35诱导的PC12细胞凋亡,提高细胞存活率,减少LDH释放,减少PC12细胞核固缩、碎裂,降低P-JNK蛋白的表达(P<0.01).结论:小剂量氯通道阻断剂Phloretin对Aβ25-35诱导的PC12细胞凋亡具有保护性抑制作用,其机制与下调JNK的磷酸化激活有关.
AIM: To investigate the inhibitive effect of chloride channel blocker phloretin on apoptosis of PC12 cells induced by Aβ25-35 (β-amyloid) and its mechanism. METHODS : PC12 cell survival and apoptosis rates in control group, Aβ25-35 group, and Aβ25-35 + phloretin group were compared by MTr assay, released lactate dehydrogenase ( LDH ) assay, Hoechst33258 staining and agarose gel electrophoresis of DNA. The expressions of JNK and P-JNK were measured by Western Blot assay. RESULTS: 10 mmol/L phloretin inhibited the apoptosis of PC12 cells induced by Aβ25-35 significantly, elevated cell survival rate, decreased the activity of the LDH, reduced karyopycnosis and caryon quassation and significantly suppressed the phosphorylation of JNK (P 〈 0.01 ). CONCLUSION: Chloride channel blocker phloretin can protect PC12 cells from apoptosis induced by Aβ25-35 through the mechanism of down-regulating JNK phosphorylation.
出处
《第四军医大学学报》
北大核心
2008年第14期1256-1258,共3页
Journal of the Fourth Military Medical University
基金
陕西省自然科学基金(2006C212)