Neuroprotection of n-Butanol Extract from Roots of Potentilla anserina on Hypoxic Injury in Primary Hippocampal Neurons |
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Authors: | QIN Xiao-jing LI Ling-zhi LV Qi YU Bao-guo YANG Shu-wang HE Tao ZHANG Yong-liang |
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Affiliation: | 1. Department of Pathology,Affiliated Hospital of Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China 2. Department of Medicinal Chemistry,Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China ;Tianjin Key Laboratory of Occupational and Environmental Hazard Biomarkers,Tianjin 300162,China 3. Department of Central Laboratory,Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China 4. Department of Rescue Medicine,Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China 5. Department of Postgraduate,Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China 6. Tianjin Key Laboratory of Occupational and Environmental Hazard Biomarkers,Tianjin 300162,China ;Logistic University of Chinese People's Armed Police Forces,Tianjin 300162,China |
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Abstract: | 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. |
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Keywords: | hypoxia mitochondria neuron Potentilla anserina ultra-microstructure |
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