Objective To investigate the protective effect of n-butanol extract from the roots of Potentilla anserina (NP) on hypoxic hippocampal neurons in neonatal rats. Methods Primary cultured hippocampal neurons were pretrea...Objective To investigate the protective effect of n-butanol extract from the roots of Potentilla anserina (NP) on hypoxic hippocampal neurons in neonatal rats. Methods Primary cultured hippocampal neurons were pretreated with different concentration of NP (0.25, 0.0625, and 0.0156 mg/mL) before incubation in a low oxygen (0.1%) environment for 4 h. Cell viability was evaluated by Trypan blue staining assay. Lactate dehydrogenase (LDH) released by neurons into the medium was measured. The activity of superoxide dismutase (SOD) in cell cytosol was determined using nitroblue tetrazolium. Morphological changes and mitochondrial function were observed by transmission electron microscopy. Results Hypoxic injury could decrease the cells viability of neuron, enhance LDH release (P < 0.05), decrease SOD activity, and increase mitochondrial injury. Pretreatment with NP significantly increased cell viability, decreased LDH release (P < 0.05), promoted SOD activity (P < 0.05), and remarkably improved cellular ultra-microstructure compared with the model group. Conclusion NP could protect the primary hippocampal neurons from hypoxic injury by attenuating mitochondrial cell death.展开更多
基金Natural Science Foundation of China (30672774 81073152)the Great Program of Science Foundation of Tianjin (10JCZDJC21100)
文摘Objective To investigate the protective effect of n-butanol extract from the roots of Potentilla anserina (NP) on hypoxic hippocampal neurons in neonatal rats. Methods Primary cultured hippocampal neurons were pretreated with different concentration of NP (0.25, 0.0625, and 0.0156 mg/mL) before incubation in a low oxygen (0.1%) environment for 4 h. Cell viability was evaluated by Trypan blue staining assay. Lactate dehydrogenase (LDH) released by neurons into the medium was measured. The activity of superoxide dismutase (SOD) in cell cytosol was determined using nitroblue tetrazolium. Morphological changes and mitochondrial function were observed by transmission electron microscopy. Results Hypoxic injury could decrease the cells viability of neuron, enhance LDH release (P < 0.05), decrease SOD activity, and increase mitochondrial injury. Pretreatment with NP significantly increased cell viability, decreased LDH release (P < 0.05), promoted SOD activity (P < 0.05), and remarkably improved cellular ultra-microstructure compared with the model group. Conclusion NP could protect the primary hippocampal neurons from hypoxic injury by attenuating mitochondrial cell death.
