目的探讨SOX2基因对人骨关节炎(OA)软骨细胞凋亡的影响及机制。方法以正常软骨组织作为对照,通过Western blotting检测OA软骨组织SOX2蛋白表达。从人OA中分离软骨细胞,参照Lipofectamine^(TM)2000说明将重组体pcDNA3.1-SOX2及空载体pcDN...目的探讨SOX2基因对人骨关节炎(OA)软骨细胞凋亡的影响及机制。方法以正常软骨组织作为对照,通过Western blotting检测OA软骨组织SOX2蛋白表达。从人OA中分离软骨细胞,参照Lipofectamine^(TM)2000说明将重组体pcDNA3.1-SOX2及空载体pcDNA3.1转染软骨细胞,并设置空白对照组。AG490作为JAK2/STAT3信号通路抑制剂,各组细胞处理48 h,通过流式细胞术、ROS试剂盒分别检测各组细胞凋亡率及ROS水平。Western blotting检测JAK2、p-JAK2、STAT3和p-STAT3的蛋白相对表达量。结果人OA软骨组织SOX2表达明显低于在正常软骨组织表达(0.065±0.009 vs 0.313±0.028,P<0.05)。转染pcDNA3.1-SOX2的OA软骨细胞SOX2表达明显高于空白组(0.556±0.048 vs 0.122±0.013,P<0.05)。pcDNA3.1-SOX2可明显降低OA软骨细胞凋亡率(3.11±0.42 vs 8.54±0.68)及ROS水平(23.46±2.15 vs 52.67±4.41),上调p-JAK2(0.142±0.013 vs 0.065±0.009)和p-STAT3表达(0.218±0.020 vs 0.126±0.015)(P<0.05),AG490(15.23±1.13 vs 8.15±0.62)可诱导OA软骨细胞凋亡,而pcDNA3.1-SOX2可减弱AG490对OA软骨细胞凋亡促进作用(P<0.05)。结论SOX2可抑制OA软骨细胞凋亡,其机制可能与激活JAK2/STAT3信号通路有关。展开更多
The Mössbauer study on mechanism of habit change has been made on KH_(2)PO_(4)(KDP)crystals grown in the presence of ^(57)Fe^(3+) iron impurities.Mössbauer spectra of the ^(57)Fe^(3+) :KDP exhibit a typical ...The Mössbauer study on mechanism of habit change has been made on KH_(2)PO_(4)(KDP)crystals grown in the presence of ^(57)Fe^(3+) iron impurities.Mössbauer spectra of the ^(57)Fe^(3+) :KDP exhibit a typical quadrupole split Fe^(3+) pattern at room temperature.The quadrupole splittingΔE(Q)=0.5lmm/s,and the isomer shift IS=0.40mm/s are obtained from computer fitting.Based on experimental results and theoretical calculation,the Fe^(3+) can occupy the interstitial positions in the lattice.展开更多
文摘目的探讨SOX2基因对人骨关节炎(OA)软骨细胞凋亡的影响及机制。方法以正常软骨组织作为对照,通过Western blotting检测OA软骨组织SOX2蛋白表达。从人OA中分离软骨细胞,参照Lipofectamine^(TM)2000说明将重组体pcDNA3.1-SOX2及空载体pcDNA3.1转染软骨细胞,并设置空白对照组。AG490作为JAK2/STAT3信号通路抑制剂,各组细胞处理48 h,通过流式细胞术、ROS试剂盒分别检测各组细胞凋亡率及ROS水平。Western blotting检测JAK2、p-JAK2、STAT3和p-STAT3的蛋白相对表达量。结果人OA软骨组织SOX2表达明显低于在正常软骨组织表达(0.065±0.009 vs 0.313±0.028,P<0.05)。转染pcDNA3.1-SOX2的OA软骨细胞SOX2表达明显高于空白组(0.556±0.048 vs 0.122±0.013,P<0.05)。pcDNA3.1-SOX2可明显降低OA软骨细胞凋亡率(3.11±0.42 vs 8.54±0.68)及ROS水平(23.46±2.15 vs 52.67±4.41),上调p-JAK2(0.142±0.013 vs 0.065±0.009)和p-STAT3表达(0.218±0.020 vs 0.126±0.015)(P<0.05),AG490(15.23±1.13 vs 8.15±0.62)可诱导OA软骨细胞凋亡,而pcDNA3.1-SOX2可减弱AG490对OA软骨细胞凋亡促进作用(P<0.05)。结论SOX2可抑制OA软骨细胞凋亡,其机制可能与激活JAK2/STAT3信号通路有关。
文摘The Mössbauer study on mechanism of habit change has been made on KH_(2)PO_(4)(KDP)crystals grown in the presence of ^(57)Fe^(3+) iron impurities.Mössbauer spectra of the ^(57)Fe^(3+) :KDP exhibit a typical quadrupole split Fe^(3+) pattern at room temperature.The quadrupole splittingΔE(Q)=0.5lmm/s,and the isomer shift IS=0.40mm/s are obtained from computer fitting.Based on experimental results and theoretical calculation,the Fe^(3+) can occupy the interstitial positions in the lattice.