女贞苷对Aβ1-42损伤SH-SY5Y细胞的保护作用及其机制

Effect of nuezhenoside to protect SH-SY5Y cell against Aβ1-42 cytotoxicity

目的:探讨女贞苷对Aβ1-42诱导神经毒性损伤SH-SY5Y细胞的保护作用及其相关作用机制.方法:对SH-SY5Y细胞进行女贞苷梯度(4μM、20μM、50μM、100μM、500μM)预保护12 h后,加入浓度为15μM的Aβ1-42诱导损伤12 h.MTT法测定终点细胞存活率,ELISA检测细胞外Aβ1-42含量,Western Blot法检测LC3表达变化.结果:女贞苷组(50μM、100μM)可明显增加细胞存活率;ELISA检测结果显示,女贞苷组细胞上清液Aβ1-42含量相较模型组下降;WB检测显示,自噬小体标记物LC3蛋白的表达下调.结论:女贞苷可有效保护Aβ1-42诱导损伤的SH-SY5Y细胞,提高细胞存活率.其可能机制为女贞苷可能增加SH-SY5Y细胞对Aβ1-42的清除,减少其在胞外的聚集而引起的神经毒性,并对自噬有一定的抑制,从而达到对细胞的保护作用.

SH-SYSY cell Aim：This study aims to investigate protective effect of nuezhenoside on Aβ1-42-induced damage and the underlying mechanism. Methods： SH-SYSY ceils were cultured with nu- ezhenoside of different concentration （4 μM ,20 μM,50μM, 100μ M,500 μM） in serum-free medium for 12 hours at 37℃ before the incubation with 15 μM Aβ1-42. Cell viability was measured by MTL LC3 expression was determined by WB, and Aβ1-42 in supernatant was determined by ELISA. Results： Nuezhenoside group （50 p^M, 100 p,M） significantly enhanced the viability of cells （ P 〈 0. 05 ）. Aβ1-42 in supernatant was decreased in treatment group compared to control group （P 〈 0. 01 ）, and lower LC3 expression was determined in treatment group. Conclusion：These results indicate that nuezhenoside can effectively protect SH-SY5Y cell from Aβ1-42 induced cytotoxicity and improve cell viability. The poten-tial mechanism is that nuezhenoside may increase Aβ1-42 and inhibit autophagy. uptaking to reduce its extracellular aggregation