Effect of sevoflurane on neurogenesis in hippocampal dentate gyrus of mice with Alzheimer′s disease
Junke Jia, Yongjuan Bao, Feng Zheng, Chang Chen, Zongze Zhang, Yufeng Zou, Ting Chen, Mian Peng, Yanlin Wang
Abstract
Junke Jia, Yongjuan Bao, Feng Zheng, Chang Chen, Zongze Zhang, Yufeng Zou, Ting Chen, Mian Peng, Yanlin Wang
Abstract
Objective To evaluate the effects of sevoflurane on neurogenesis in hippocampal dentate gyrus(DG)of mice with Alzheimer′s disease. Methods Thirty-six SPF male APP/PS1 mice, aged 8 months, weighing 30-35 g, were divided into 3 groups(n=12 each)using a random number table: Alzheimer′s disease group(group AD), oxygen group(group O2)and sevoflurane group(group Sev). Another 12 wild-type mice served as control group(group C). In group Sev, 3.0% sevoflurane was inhaled for 2 h once a day for 3 consecutive days.The mixture of air and oxygen was inhaled in group O2.Morris water maze test was performed on 22 to 28 days after the last sevoflurane inhalation.Then the mice were sacrificed and hippocampi were isolated for determination of doublecortin(DCX)positive cell count(by immunohistochemistry)and neuronal nuclei(NeuN)/5-bromo-2′-deoxyuridine(BrdU)and glial fibrillary acidic protein(GFAP)/BrdU positive cell count in hippocampal DG(by immunofluorescence). Results Compared with group C, the escape latency was significantly prolonged, the percentage of time spent in the target quadrant was decreased, and DCX, NeuN/BrdU and GFAP/BrdU positive cell counts were reduced in AD, O2 and Sev groups(P 0.05). Compared with group O2, the escape latency was significantly prolonged, the percentage of time spent in the target quadrant was decreased, and DCX, NeuN/BrdU and GFAP/BrdU positive cell counts were reduced in group Sev(P<0.05). Conclusion Sevoflurane leads to cognitive decline through depressing neurogenesis in hippocampal DG of mice with Alzheimer′s disease. Key words: Anesthetics, inhalation; Alzheimer′s disease; Hippocampus; Neurogenesis
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Objective To evaluate the effects of sevoflurane on neurogenesis in hippocampal dentate gyrus(DG)of mice with Alzheimer′s disease. Methods Thirty-six SPF male APP/PS1 mice, aged 8 months, weighing 30-35 g, were divided into 3 groups(n=12 each)using a random number table: Alzheimer′s disease group(group AD), oxygen group(group O2)and sevoflurane group(group Sev). Another 12 wild-type mice served as control group(group C). In group Sev, 3.0% sevoflurane was inhaled for 2 h once a day for 3 consecutive days.The mixture of air and oxygen was inhaled in group O2.Morris water maze test was performed on 22 to 28 days after the last sevoflurane inhalation.Then the mice were sacrificed and hippocampi were isolated for determination of doublecortin(DCX)positive cell count(by immunohistochemistry)and neuronal nuclei(NeuN)/5-bromo-2′-deoxyuridine(BrdU)and glial fibrillary acidic protein(GFAP)/BrdU positive cell count in hippocampal DG(by immunofluorescence). Results Compared with group C, the escape latency was significantly prolonged, the percentage of time spent in the target quadrant was decreased, and DCX, NeuN/BrdU and GFAP/BrdU positive cell counts were reduced in AD, O2 and Sev groups(P 0.05). Compared with group O2, the escape latency was significantly prolonged, the percentage of time spent in the target quadrant was decreased, and DCX, NeuN/BrdU and GFAP/BrdU positive cell counts were reduced in group Sev(P<0.05). Conclusion Sevoflurane leads to cognitive decline through depressing neurogenesis in hippocampal DG of mice with Alzheimer′s disease. Key words: Anesthetics, inhalation; Alzheimer′s disease; Hippocampus; Neurogenesis
Key concepts: NeuN, Dentate gyrus, Hippocampal formation, Doublecortin, Neurogenesis, Glial fibrillary acidic protein, Hippocampus, Sevoflurane