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目的观察桑椹提取物(ME)对β-淀粉样蛋白(Aβ25-35)致PC12细胞损伤的保护作用,并初步探讨相关机制。方法将细胞分为对照组(未加任何处理因素)、Aβ25-35组(20μmol/L Aβ25-35损伤24h)以及(25、50、100、200、400和800μg/ml)ME预孵育组(ME预孵育24h后再给予20μmol/L Aβ25-35继续损伤24h),采用MTT法确定ME的干预浓度。在此基础上,将细胞分为对照组(未加任何处理因素)、ME组(200μg/ml ME作用24h)、Aβ25-35组(20μmol/L Aβ25-35损伤24h)以及ME预孵育+Aβ25-35组(200μg/ml ME预孵育24h后再给予20μmol/L Aβ25-35继续损伤24h),采用分子探针DCFH-DA及Hoechst33342染色法分别进行细胞内活性氧(ROS)含量及细胞凋亡的测定。结果 (1)与对照组相比,Aβ25-35组细胞存活率显著降低(P<0.05);与Aβ25-35组相比,100、200μg/ml ME预孵育组细胞存活率显著提高(P<0.05)。(2)与对照组相比,200μg/ml ME组细胞ROS的生成及细胞凋亡率无显著变化(P>0.05),而Aβ25-35组细胞内ROS的生成显著升高(P<0.05)、细胞凋亡率也明显增加(P<0.05);与Aβ25-35组相比,200μg/ml ME预孵育组细胞内ROS的生成显著减少(P<0.05)且细胞凋亡率明显降低(P<0.05)。结论桑椹提取物对Aβ25-35致PC12细胞损伤有明显的保护作用,机制与其抗氧化及抑制凋亡作用有关。
Objective To observe the protective effect of mulberry extract (ME) on the injury of PC12 cells induced by β-amyloid protein (Aβ25-35) and to explore the underlying mechanisms. Methods The cells were divided into control group (without any treatment), Aβ25-35 group (20μmol / L Aβ25-35 injury 24h) and (25,50,100,200,400 and 800μg / ml ME preincubation group ME pre-incubated 24h and then given 20μmol / L Aβ25-35 continue to damage 24h), MTT method to determine the intervention concentration of ME. On this basis, the cells were divided into control group (without any treatment factor), ME group (200μg / ml ME for 24h), Aβ25-35 group (20μmol / L Aβ25-35 injury 24h) and ME preincubation + Aβ25 -35 group (200μg / ml ME preincubated 24h and then given 20μmol / L Aβ25-35 continue to damage 24h), using molecular probe DCFH-DA and Hoechst33342 staining were intracellular reactive oxygen species (ROS) content and apoptosis The determination. Results (1) The cell viability in Aβ25-35 group was significantly lower than that in control group (P <0.05). Compared with Aβ25-35 group, the survival rate of cells pre-incubated with 100 and 200μg / ml ME was significantly increased (P < 0.05). (2) Compared with the control group, the generation of ROS and the rate of apoptosis did not change in 200μg / ml ME group (P> 0.05), while the production of ROS in Aβ25-35 group was significantly increased (P <0.05) (P <0.05). Compared with Aβ25-35 group, the production of ROS in 200μg / ml ME pre-incubation group was significantly decreased (P <0.05) and the apoptosis rate was significantly decreased (P <0.05) <0.05). Conclusion Mulberry extract has a significant protective effect on Aβ25-35 induced PC12 cell injury, and its mechanism is related to its anti-oxidation and anti-apoptotic effects.