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作 者:李娜[1,2] 蔡珂沁 李文欣 吕军[1] 石瑞丽[1] 马宝慧[1] 时静华[1] 郝肖琼 邵国 齐瑞芳[1,2] LI Na;CAI Ke-qin;LI Wen-xin;LYU Jun;SHI Rui-li;MA Bao-hui;SHI Jing-hua;HAO Xiao-qiong;SHAO Guo;QI Rui-fang(School of Basic Medicine and Forensic Sciences,Baotou Medical College of Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014040,China;Inner Mongolia Key Laboratory of Hypoxic Adaptive Translational Medicine,Baotou Medical College of Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014040,China;Centre for Translational Medicine,the Third People′s Hospital of Longgang District of Shenzhen,Shenzhen 518172,China)
机构地区:[1]内蒙古科技大学包头医学院基础医学与法医学院,内蒙古包头014040 [2]内蒙古科技大学包头医学院内蒙古低氧适应转化医学重点实验室,内蒙古包头014040 [3]广东省深圳市龙岗区第三人民医院转化医学中心,广东深圳518172
出 处:《中国药理学通报》2023年第8期1522-1526,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 82060337);内蒙古自治区高等学校科学研究项目(No NJZY20171);包头医学院科学研究基金项目(No BYJJ-BSJJ-202003)。
摘 要:目的研究丙酮酸钠(sodium pyruvate,SP)在低氧条件下对小鼠海马神经细胞HT22的神经保护作用。方法在低氧条件下,用MTS检测不同浓度SP孵育HT22细胞的活性变化;从形态学上,采用铁染色观察SP对HT22细胞的影响;应用溶酶体染色检测SP对HT22细胞的溶酶体变化;采用Western blot检测Bcl-2、Bax和LC3-Ⅱ/LC3-Ⅰ蛋白的表达。结果5 mmol·L^(-1)的SP能提高HT22细胞活力以及减少HT22细胞损伤;SP提高Bcl-2的表达,降低Bax的表达,使LC3-Ⅱ/LC3-Ⅰ比值增加。结论在低氧的条件下给予SP可能通过减少HT22细胞凋亡,激活自噬发挥神经保护作用,从而降低低氧损伤。Aim To study the effect of sodium pyruvate on apoptosis and autophagy of HT22 in mouse hippocampal neuronal cells under hypoxia conditions.Methods HT22 cells were incubated with different concentrations of sodium pyruvate to detect their cellular activity by MTS;iron staining was used to further observe the effect of sodium pyruvate on HT22 cells in mitochondrial metabolism;lysosomal staining was applied to detect the lysosomal changes of sodium pyruvate on HT22 cells;Western blot was used to detect the expression of Bcl-2,Bax and LC3-II/LC3-Ⅰ proteins.Results To verify whether sodium pyruvate exerted neuroprotective effects on mouse hippocampal HT22 cells through affecting mitochondrial apoptosis and autophagy pathways,which were improved by administration of sodium pyruvate.Conclusions Sodium pyruvate administration under hypoxic conditions can reduce the neuroprotective effect of hypoxic injury by reducing apoptosis and activating autophagy in HT22 cells.
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