褪黑素在铅致神经细胞毒性中的保护作用

Objective To study the protective effect of melatonin (MT) against lead-induced neurotoxicity. Methods PC12 cells were divided in four groups(control, 25 滋mol/L PbAc, 50 滋mol/L MT and 25 滋mol/L PbAc+50 滋mol/L MT). After treatment, cell viability was detected by cell counting kit-8(CCK-8) assay and cytotoxicity LDH assay were used to evaluate cell damage rate. The expression of Cleaved-Caspase-3 and cytochrome C (cyto C) was detected by immunofluorescence (IF). ROS levels were measured by DCFH method. GSH contents and SOD activities were detected after whole cell protein was extracted. Results Compared with control group, 25 滋mol/L PbAc caused significantly decreased cell viability, GSH contents and SOD activities, while increased cell damage rate and ROS level significantly (P<0.05). 25 滋mol/L PbAc could also increase the protein level of cleaved-caspase-3 and cyto C in cytoplasm. Compared with 25 滋mol/L PbAc group, 50 滋mol/L MT+25 滋mol/L PbAc caused significantly increased cell viability, GSH contents and SOD activities, while decreased cell damage rate and ROS level significantly (P<0.05). Compared with 25 滋mol/L PbAc group, 50 滋mol/L MT+25 滋mol/L PbAc decreased the protein level of cleaved-caspase-3 and cyto C. Conclusion Melatonin could attenuate PbAc-induced oxidative stress and cell death and promote cell survival.