[Primary study on protective effect of mulberry extracts on Abeta25-35-induced PC12 cells injury]

To investigate the neuroprotective effect of mulberry extracts (ME) against Abeta25-35-induced injury in cultured PC12 cells and explore the possible mechanisms involved.

PC12 cells at logarithmic growth phase were divided into the normal control group, Abeta25-35 group (20 micromol/L for 24h) and ME pretreating groups at the concentrations of 25, 50, 100, 200, 400, 800 microg/ml. Cell viability was determined by MTT assay. On that basis, PC12 cells were divided into the normal control group, ME group (200 microg/ml ME incubation alone for 24h), Abeta25-35 group (20 micromol/L for 24h) and ME plus Abeta25-35 group (after pretreatment with 200 microg/ml ME for 24h, cells were exposed to 201 micromol/L Abeta25-35 for another 24h). Intracellular reactive oxidative species (ROS) was measured by using the fluorescent DCFH-DA and the apoptotic cells were observed by Hoechst33342 staining method.

(1) The results showed that exposure of PC12 cells to Abeta22-35 (20 micromol/L) for 24h induced notably neuronal injury (P < 0.05) as compared with the control group, while pretreatment with 100 or 200 microg/ml ME almost completely reversed Abeta25-35 induced neuronal injury (P < 0.05). (2) There were no remarkable changes in ROS levels and apoptosis rate of ME group as compared with the control group (P > 0.05). Compared with the control group, exposure to 20 micromol/L Abeta25-35 for 24h resulted in a significant decrease in cell viability (P < 0.05) while increase in ROS levels and cell apoptosis rate (P < 0.05). But pretreatment of PC12 cells with 200 microg/ml ME could counteract ROS formation and inhibit apoptosis (P < 0.05).

These results suggest that mulberry extracts rich in phenolics and anthocyanins could alleviate Abeta25-35-induced injury in PC12 cells, which might be associated with the antioxidative and antiapoptosis effects.