A combination of HBr and trans-3,5-dihydroperoxy-3,5-dimethyl-1,2-dioxolane as anew and powerful oxidant was found effective for facile brotnination of different aromatic compounds at room temperature in water as a gr...A combination of HBr and trans-3,5-dihydroperoxy-3,5-dimethyl-1,2-dioxolane as anew and powerful oxidant was found effective for facile brotnination of different aromatic compounds at room temperature in water as a green solvent.Mild reaction conditions,high selectivity and yield,high reaction rate and non-toxicity are some of the major advantages of this synthetic protocol.展开更多
The title compound trans-4-[（5-（2,4-dichlorophenoxy）-3-methyl- 1-phenyl-1H-pyrazol-4-yl）methyleneamino]- 1,5-dimethyl-2-phenyl-1,2-dihydropyrazol-3-one 3 （C28H23Cl2N5O2, Mr = 532.41） has been synthesized and its...The title compound trans-4-[（5-（2,4-dichlorophenoxy）-3-methyl- 1-phenyl-1H-pyrazol-4-yl）methyleneamino]- 1,5-dimethyl-2-phenyl-1,2-dihydropyrazol-3-one 3 （C28H23Cl2N5O2, Mr = 532.41） has been synthesized and its crystal structure was determined by single-crystal X-ray diffraction analysis. It crystallizes in triclinic, space group P1- with a = 8.9438（4）, b = 11.6065（5）, c = 14.2215（6）A, α = 112.566（1）, β = 92.324（2）, γ = 102.91（1）°, V= 1315.65（10） A^3, Z = 2, Dc = 1.344 g/cm^3,μ（MoKa） = 0.282 mm^-1, λ = 0.71073 A, F（000） = 552, the final R = 0.0587 and wR = 0.1578 for 5071 observed reflections （I 〉 2σ（I））. X-ray analysis reveals that the product is a thermodynamically stable trans isomer. Intra- and intermolecular C（ 12）-H（12）…O（1） and C（28）-H（28）...O（1）# 1 hydrogen bonds were observed in the title compound.展开更多
The title compound, Cs 2[Mg(CO 3) 2(H 2O) 4], was synthesized by the dropwise addition of an aqueous solution of Mg(NO 3) 2 to a stirred aqueous Cs 2CO 3/CsHCO 3 solution. A colorless needle shaped crystal was formed ...The title compound, Cs 2[Mg(CO 3) 2(H 2O) 4], was synthesized by the dropwise addition of an aqueous solution of Mg(NO 3) 2 to a stirred aqueous Cs 2CO 3/CsHCO 3 solution. A colorless needle shaped crystal was formed by slow evaporation. The crystal structure was established on the basis of the single crystal X ray diffraction data. Cs 2[Mg(CO 3) 2(H 2O) 4] crystallized in the orthorhombic space group Pbca (No. 61) with a =0.658 4(1) nm, b =1.257 9(1) nm, c =1.301 3(1) nm, \{ V =1.077 8 nm 3, Z =4, D x=2.971 g·cm -3 , μ =69.20 cm -1 , F (000)=888, T =298 K, final R =0.029 and R w=0.024 for 1 037 observed reflections. The crystal consists of Cs + cations and the complex trans [Mg(CO 3) 2(H 2O) 4] 2- anions with each Mg atom coordinated by the six oxygens of two carbonate groups and four water molecules [ d (Mg_O)=0.203 6(4), 0.207 4(4), 0.213 4(4) nm]. The complex trans [Mg(CO 3) 2(H 2O) 4] 2- anions are arranged in a strongly compressed bcc pattern. A 3D network was formed through the intermolecular hydrogen bonds. The Cs + cations are located in cavities, each being surrounded by nine oxygens of five complex anions with d (Cs_O)=0.306 1-0.348 8 nm. The CO 2- 3 group reveals a lowering of D 3h symmetry due to site and coordination effects, but not any observable deviation from co planarity [ d (C_O)=0.127 2(6), 0.127 5(7) , 0.130 5(6) nm and O_C_O=119.6(5)°, 120.1(5)°, 120.4(5)°].展开更多
目的:探讨转录因子腺病毒E4启动子结合蛋白(adenovirus E4 promoter-binding protein,E4BP4)通过腺苷酸活化蛋白激酶(adenosine monophosphate-activated protein kinase,AMPK)-转化生长因子(transforming growth factor,TGF)-β1/SMAD...目的:探讨转录因子腺病毒E4启动子结合蛋白(adenovirus E4 promoter-binding protein,E4BP4)通过腺苷酸活化蛋白激酶(adenosine monophosphate-activated protein kinase,AMPK)-转化生长因子(transforming growth factor,TGF)-β1/SMAD同源物3(Smad homolog 3,SMAD3)通路在调控病理性心肌纤维化的作用。方法:建立小鼠心脏纤维化模型,分别于模型组和假手术组中检测E4BP4的表达差异。分离和培养原代心脏成纤维细胞,血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)刺激增殖活化,分别转染E4BP4过表达质粒(Ang Ⅱ+E4BP4组)、E4BP4干扰质粒(Ang Ⅱ+siE4BP4组)、Ang Ⅱ组和未经Ang Ⅱ处理的对照组。免疫荧光检测α-肌动蛋白(α-smooth muscle actin,α-SMA)荧光强度,细胞增殖检测试剂盒测定细胞活力,聚合酶链式反应检测E4BP4、α-SMA、Ⅰ型胶原蛋白(collagen type Ⅰ,Collagen Ⅰ)和Ⅲ型胶原蛋白(collagen type Ⅲ,Collagen Ⅲ)的表达,蛋白质印迹检测TGF-β1、AMPK和SMAD3的蛋白表达。结果:与假手术组比较,模型组心肌纤维化程度(38.46±1.21 vs. 3.39±0.39,t=-78.564,P=0.000)、E4BP4蛋白表达量(0.96±0.03 vs. 0.75±0.03,t=-11.480,P=0.000)均明显增加。体外实验发现,与Ang Ⅱ+E4BP4组比较,Ang Ⅱ+siE4BP4组在平均荧光强度(0.05±0.01 vs. 0.42±0.03,F=677.591,P=0.000)、细胞活力(91.30±2.39vs.123.74±2.60,F=132.696,P=0.000)、α-SMA(1.26±0.09vs.3.59±0.86,F=52.274,P=0.000)、Collagen Ⅰ(1.16±0.11vs.3.79±0.89,F=55.336,P=0.000)、Collagen Ⅲ(1.23±0.13 vs. 2.92±0.36,F=119.929,P=0.000)、TGF-β1(0.66±0.04 vs. 0.96±0.02,F=142.954,P=0.000)和p-SMAD3/SMAD3(0.81±0.03 vs. 1.37±0.02,F=739.609,P=0.000)的水平明显降低,而p-AMPK/AMPK的表达量在Ang Ⅱ+siE4BP4组明显高于Ang Ⅱ+E4BP4组(0.89±0.01 vs. 0.58±0.02,F=284.541,P=0.000)。结论:E4BP4是纤维化调控的关键因子,抑制其表达可通过激活AMPK进而抑制TGF-β1/SMAD3通路发挥抗纤维化作用。展开更多
目的探讨细胞因子信号转导抑制因子3(suppressors of cytokine signaling 3,SOCS3)过表达对实验性自身免疫性心肌炎(experimental autoimmune myocarditis,EAM)大鼠CD4^(+)T细胞失衡的影响及机制。方法从30只雄性Lewis大鼠中随机选取10...目的探讨细胞因子信号转导抑制因子3(suppressors of cytokine signaling 3,SOCS3)过表达对实验性自身免疫性心肌炎(experimental autoimmune myocarditis,EAM)大鼠CD4^(+)T细胞失衡的影响及机制。方法从30只雄性Lewis大鼠中随机选取10只作为对照组,其余20只大鼠在实验第0天和第7天注射猪心肌肌球蛋白,建立EAM大鼠模型。将20只大鼠随机分为EAM组和EAM+SOCS3组。EAM+SOCS3组尾静脉注射过表达SOCS3慢病毒,EAM组尾静脉注射等量空载体慢病毒。实验第21天对所有大鼠进行超声心动图检查,评估其心脏功能后实施安乐死。采用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)法检测血清心肌肌钙蛋白T、肌酸激酶同工酶、B型利钠肽和血清细胞因子水平。采用苏木精-伊红(hematoxylin-eosin,HE)染色法评估心肌组织炎症浸润和心肌病理积分,流式细胞仪检测大鼠脾脏中CD4^(+)T细胞亚群水平。采用实时荧光定量聚合酶链反应(real time fluorescent quantitative polymerase chain reaction,RT-qPCR)法和蛋白质印迹(Western blot,WB)法检测SOCS3、Janus激酶2(Janus kinase 2,JAK2)、信号转导和转录激活因子3(signal transducer and activator of transcription 3,STAT3)和CD4^(+)T细胞特异性转录因子的表达。结果EAM组血清心肌肌钙蛋白T、肌酸激酶同工酶、B型利钠肽的表达水平较对照组上升(P<0.05),心肌病理积分较对照组上升(P<0.05);EAM组心肌组织中T细胞转录因子(T-box expressed in T cells,T-bet)、维甲酸相关孤核受体γt(retinoid-related orphan receptorγt,RORγt)mRNA和蛋白表达水平较对照组上升(P<0.05),叉状头转录因子P3(forkhead box P3,Foxp3)表达水平下降(P<0.05);EAM组脾脏中辅助性T细胞1(helper T cell 1,Th1)、辅助性T细胞17(helper T cell 17,Th17)百分比较对照组上升(P<0.05),调节性T细胞(regulatory T cell,Treg)百分比下降(P<0.05);EAM组心肌组织中JAK2、STAT3mRNA和蛋白的表达水平较对照组上升(P<0.05)。EAM+SOCS3组这些指标较EAM均有不同程度的恢复(P<0.05)。结论SOCS3过表达可改善EAM大鼠CD4^(+)T细胞失衡,减轻心肌损害,其机制可能与下调JAK2/STAT3信号通路有关。展开更多
文摘A combination of HBr and trans-3,5-dihydroperoxy-3,5-dimethyl-1,2-dioxolane as anew and powerful oxidant was found effective for facile brotnination of different aromatic compounds at room temperature in water as a green solvent.Mild reaction conditions,high selectivity and yield,high reaction rate and non-toxicity are some of the major advantages of this synthetic protocol.
基金the Science Research Foundation of Henan Institute of Science and Technology (No. 06036)
文摘The title compound trans-4-[（5-（2,4-dichlorophenoxy）-3-methyl- 1-phenyl-1H-pyrazol-4-yl）methyleneamino]- 1,5-dimethyl-2-phenyl-1,2-dihydropyrazol-3-one 3 （C28H23Cl2N5O2, Mr = 532.41） has been synthesized and its crystal structure was determined by single-crystal X-ray diffraction analysis. It crystallizes in triclinic, space group P1- with a = 8.9438（4）, b = 11.6065（5）, c = 14.2215（6）A, α = 112.566（1）, β = 92.324（2）, γ = 102.91（1）°, V= 1315.65（10） A^3, Z = 2, Dc = 1.344 g/cm^3,μ（MoKa） = 0.282 mm^-1, λ = 0.71073 A, F（000） = 552, the final R = 0.0587 and wR = 0.1578 for 5071 observed reflections （I 〉 2σ（I））. X-ray analysis reveals that the product is a thermodynamically stable trans isomer. Intra- and intermolecular C（ 12）-H（12）…O（1） and C（28）-H（28）...O（1）# 1 hydrogen bonds were observed in the title compound.
文摘The title compound, Cs 2[Mg(CO 3) 2(H 2O) 4], was synthesized by the dropwise addition of an aqueous solution of Mg(NO 3) 2 to a stirred aqueous Cs 2CO 3/CsHCO 3 solution. A colorless needle shaped crystal was formed by slow evaporation. The crystal structure was established on the basis of the single crystal X ray diffraction data. Cs 2[Mg(CO 3) 2(H 2O) 4] crystallized in the orthorhombic space group Pbca (No. 61) with a =0.658 4(1) nm, b =1.257 9(1) nm, c =1.301 3(1) nm, \{ V =1.077 8 nm 3, Z =4, D x=2.971 g·cm -3 , μ =69.20 cm -1 , F (000)=888, T =298 K, final R =0.029 and R w=0.024 for 1 037 observed reflections. The crystal consists of Cs + cations and the complex trans [Mg(CO 3) 2(H 2O) 4] 2- anions with each Mg atom coordinated by the six oxygens of two carbonate groups and four water molecules [ d (Mg_O)=0.203 6(4), 0.207 4(4), 0.213 4(4) nm]. The complex trans [Mg(CO 3) 2(H 2O) 4] 2- anions are arranged in a strongly compressed bcc pattern. A 3D network was formed through the intermolecular hydrogen bonds. The Cs + cations are located in cavities, each being surrounded by nine oxygens of five complex anions with d (Cs_O)=0.306 1-0.348 8 nm. The CO 2- 3 group reveals a lowering of D 3h symmetry due to site and coordination effects, but not any observable deviation from co planarity [ d (C_O)=0.127 2(6), 0.127 5(7) , 0.130 5(6) nm and O_C_O=119.6(5)°, 120.1(5)°, 120.4(5)°].
文摘目的:探讨转录因子腺病毒E4启动子结合蛋白(adenovirus E4 promoter-binding protein,E4BP4)通过腺苷酸活化蛋白激酶(adenosine monophosphate-activated protein kinase,AMPK)-转化生长因子(transforming growth factor,TGF)-β1/SMAD同源物3(Smad homolog 3,SMAD3)通路在调控病理性心肌纤维化的作用。方法:建立小鼠心脏纤维化模型,分别于模型组和假手术组中检测E4BP4的表达差异。分离和培养原代心脏成纤维细胞,血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)刺激增殖活化,分别转染E4BP4过表达质粒(Ang Ⅱ+E4BP4组)、E4BP4干扰质粒(Ang Ⅱ+siE4BP4组)、Ang Ⅱ组和未经Ang Ⅱ处理的对照组。免疫荧光检测α-肌动蛋白(α-smooth muscle actin,α-SMA)荧光强度,细胞增殖检测试剂盒测定细胞活力,聚合酶链式反应检测E4BP4、α-SMA、Ⅰ型胶原蛋白(collagen type Ⅰ,Collagen Ⅰ)和Ⅲ型胶原蛋白(collagen type Ⅲ,Collagen Ⅲ)的表达,蛋白质印迹检测TGF-β1、AMPK和SMAD3的蛋白表达。结果:与假手术组比较,模型组心肌纤维化程度(38.46±1.21 vs. 3.39±0.39,t=-78.564,P=0.000)、E4BP4蛋白表达量(0.96±0.03 vs. 0.75±0.03,t=-11.480,P=0.000)均明显增加。体外实验发现,与Ang Ⅱ+E4BP4组比较,Ang Ⅱ+siE4BP4组在平均荧光强度(0.05±0.01 vs. 0.42±0.03,F=677.591,P=0.000)、细胞活力(91.30±2.39vs.123.74±2.60,F=132.696,P=0.000)、α-SMA(1.26±0.09vs.3.59±0.86,F=52.274,P=0.000)、Collagen Ⅰ(1.16±0.11vs.3.79±0.89,F=55.336,P=0.000)、Collagen Ⅲ(1.23±0.13 vs. 2.92±0.36,F=119.929,P=0.000)、TGF-β1(0.66±0.04 vs. 0.96±0.02,F=142.954,P=0.000)和p-SMAD3/SMAD3(0.81±0.03 vs. 1.37±0.02,F=739.609,P=0.000)的水平明显降低,而p-AMPK/AMPK的表达量在Ang Ⅱ+siE4BP4组明显高于Ang Ⅱ+E4BP4组(0.89±0.01 vs. 0.58±0.02,F=284.541,P=0.000)。结论:E4BP4是纤维化调控的关键因子,抑制其表达可通过激活AMPK进而抑制TGF-β1/SMAD3通路发挥抗纤维化作用。
文摘目的探讨细胞因子信号转导抑制因子3(suppressors of cytokine signaling 3,SOCS3)过表达对实验性自身免疫性心肌炎(experimental autoimmune myocarditis,EAM)大鼠CD4^(+)T细胞失衡的影响及机制。方法从30只雄性Lewis大鼠中随机选取10只作为对照组,其余20只大鼠在实验第0天和第7天注射猪心肌肌球蛋白,建立EAM大鼠模型。将20只大鼠随机分为EAM组和EAM+SOCS3组。EAM+SOCS3组尾静脉注射过表达SOCS3慢病毒,EAM组尾静脉注射等量空载体慢病毒。实验第21天对所有大鼠进行超声心动图检查,评估其心脏功能后实施安乐死。采用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)法检测血清心肌肌钙蛋白T、肌酸激酶同工酶、B型利钠肽和血清细胞因子水平。采用苏木精-伊红(hematoxylin-eosin,HE)染色法评估心肌组织炎症浸润和心肌病理积分,流式细胞仪检测大鼠脾脏中CD4^(+)T细胞亚群水平。采用实时荧光定量聚合酶链反应(real time fluorescent quantitative polymerase chain reaction,RT-qPCR)法和蛋白质印迹(Western blot,WB)法检测SOCS3、Janus激酶2(Janus kinase 2,JAK2)、信号转导和转录激活因子3(signal transducer and activator of transcription 3,STAT3)和CD4^(+)T细胞特异性转录因子的表达。结果EAM组血清心肌肌钙蛋白T、肌酸激酶同工酶、B型利钠肽的表达水平较对照组上升(P<0.05),心肌病理积分较对照组上升(P<0.05);EAM组心肌组织中T细胞转录因子(T-box expressed in T cells,T-bet)、维甲酸相关孤核受体γt(retinoid-related orphan receptorγt,RORγt)mRNA和蛋白表达水平较对照组上升(P<0.05),叉状头转录因子P3(forkhead box P3,Foxp3)表达水平下降(P<0.05);EAM组脾脏中辅助性T细胞1(helper T cell 1,Th1)、辅助性T细胞17(helper T cell 17,Th17)百分比较对照组上升(P<0.05),调节性T细胞(regulatory T cell,Treg)百分比下降(P<0.05);EAM组心肌组织中JAK2、STAT3mRNA和蛋白的表达水平较对照组上升(P<0.05)。EAM+SOCS3组这些指标较EAM均有不同程度的恢复(P<0.05)。结论SOCS3过表达可改善EAM大鼠CD4^(+)T细胞失衡,减轻心肌损害,其机制可能与下调JAK2/STAT3信号通路有关。
