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作 者:庞安然 应航[1] PANG Anran;YING Hang(Zhejiang Chinese Medical University,Hangzhou 310053,China)
出 处:《中华耳科学杂志》2022年第2期300-305,共6页Chinese Journal of Otology
基 金:浙江省公益计划研究项目(项目编号:LGF19H170002)~~。
摘 要:目的 探究酸敏感离子通道1a(Acid-sensing ion channel 1a,ASIC1a)在缺氧/复氧所致小鼠听觉皮层星形胶质细胞增殖中的作用。方法 参照氧糖剥夺/再复氧(Oxygen and glucose deprivation/reoxygenation, OGD/R)模型,模拟缺血性中风的病理过程;将野生型C57BL/6j与Asic1a敲除的小鼠原代培养的听觉皮层星形胶质细胞分为常氧组和缺氧组,同时常氧组和缺氧组又分别分为无糖组和有糖组;上述各组细胞运用免疫荧光、免疫印迹法测定ASIC1a蛋白的表达量;采用CCK-8试剂盒、EdU试剂盒检测各组细胞的增殖情况。结果 与常氧组相比,缺氧组听觉皮层星形胶质细胞ASIC1a蛋白的表达量显著增加(F=21.72;P<0.001);与野生型小鼠相比,Asic1a敲除小鼠缺氧无糖组听觉皮层星形胶质细胞在缺氧/复氧后增殖增加(t=-2.275;P=0.035),缺氧有糖组增殖显著增加(t=10.244;P<0.001)。结论 缺氧/复氧后酸敏感离子通道蛋白表达量的增加抑制了小鼠听觉皮层星形胶质细胞的增殖。Objective To investigate the role of acid-sensing ion channel 1a(ASIC1a) in the proliferation of astrocytes induced by hypoxia/reoxygenation in mice auditory cortex. Methods An in vivo Oxygen and glucose deprivation/reoxygenation(OGD/R) model was used to simulate the pathological process of ischemia-reperfusion. Cortical astrocytes were divided into a normoxia and a hypoxia group, which were further divided into glucose-free and glucosecontaining subgroups, respectively. Cell proliferation was detected using the CCK-8 and EdU kits and expression of the ASIC1a channel protein was determined by immunofluorescence and western blotting. Results Compared with the normoxia group, expression of the ASIC1a protein in auditory cortex astrocytes in the hypoxia group was significantly increased(F=21.72;P<0.001). Astrocytes in the auditory cortex increased significantly after hypoxia/reoxygenation in the oxygen and glucose-free group(t=-2.275;P=0.035), and in the hypoxia and glucose group(t=10.244;P<0.001). Conclusion Increase of acid-sensing ion channel protein expression after hypoxia/reoxygenation inhibits the proliferation of mouse auditory cortex astrocytes.
关 键 词:听觉皮层 星形胶质细胞 酸敏感离子通道 缺氧/复氧
分 类 号:R764[医药卫生—耳鼻咽喉科]
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