Poly[ 2, 2-（m.phenylene） -5, 5-bibenzimidazole] （mPBI） were synthesized by mixing 3, 3＇, 4, 4＇-tetraaminobiphenyl and isophthallc acid in 1 -butyl-3 -methyUmidazolinm chloride （ E BMIM] CI）. Intrinsic viscosit...Poly[ 2, 2-（m.phenylene） -5, 5-bibenzimidazole] （mPBI） were synthesized by mixing 3, 3＇, 4, 4＇-tetraaminobiphenyl and isophthallc acid in 1 -butyl-3 -methyUmidazolinm chloride （ E BMIM] CI）. Intrinsic viscosity of mPBI polymers was 0.67 dL/g which was measured in 96% sulfuric acid. The polymer was characterized by Fourier transform infrared spectroscopy （FTIR）, nuclear magnetic resonance （ 1H-NMR ）, and thermogravimetric analysis （TGA）. The effects of polymerization conditions on the intrinsic viscosity of mPBI were investigated. It showed that the molecular weight of polymer mainly depended on pre-reaction time and reaction temperature. Comparison of structure and properties of mPBI synthesized in ionic liquids（ILs） and polyphosphoric acid was also reported. It indicates that the ionic liquids are a kind of good solvents in synthesis process of m_PBI and ionic liquids mainly affect molecular weight of mPBL展开更多
Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic ...Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2＇-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor.展开更多
Aim Angiotensin II （AngII） induces vascular smooth muscle cell （VSMC） migration and growth, which is responsible for vascular remodeling during some cardiovascular diseases. It has been demonstrated to activate a ...Aim Angiotensin II （AngII） induces vascular smooth muscle cell （VSMC） migration and growth, which is responsible for vascular remodeling during some cardiovascular diseases. It has been demonstrated to activate a C1 current, but the underlying mechanism is not clear. Methods Whole-cell patch clamp, co-immunoprecipitation （co-IP）, site-specific mutagenesis, angiotensinII-infusion hypertensive mice model were used. Results In VSMCs, AngII could induce a C1C-3-dependent C1- current that was abolished in C1C-3 null mice. The activation mechanism of this AngII-induced C1- current was ascribed to the interaction between C1C-3 and Rho-kinase 2 （ROCIL2）, as re- vealed by N-terminal or C-terminal truncation of C1C-3, ROCIC2 siRNA and Co-IP experiments. Then we searched for and identified the phosphorylation site of C1C-3 at threonine 532 is critical for AngII-induced C1- current and VSMC migration through ROCK. The C1C-3 T532D mutant （mutation of threonine 532 to aspartate）, mimicking the phos- phorylation state of C1C-3, significantly potentiated AngII-induced C1- current and VSMC migration; while C1C-3 T532A （mutation of threonine 532 to alanine） had the opposite effects. Furthermore, we found a remarkably de- creased AngII-induced VSMC migration in C1C-3 null mice that is insensitive to Y27632, an inhibitor of ROCIL2. In addition, AngII-induced cerebrovascular remodeling was ameliorated in C1C-3 null mice, possibly by ROCIL2 path- way. Conclusions C1C-3 protein phosphorylation at threonine 532 by ROCIL2 is required for AngII-induced C1- cur- rent and VSMC migration that are involved in AngII-induced hypertensive vascular remodeling.展开更多
1,1,1,-Trifluoro-2- substituted- phenyl- 2- propanols- 3- 14C were prepared from addition of methyl- 14C magnesium iodide to appropriate trifluoroacetophenone. These alcohols were converted into tosylatcs by reaction ...1,1,1,-Trifluoro-2- substituted- phenyl- 2- propanols- 3- 14C were prepared from addition of methyl- 14C magnesium iodide to appropriate trifluoroacetophenone. These alcohols were converted into tosylatcs by reaction with n-butyllithium and then with p-toluenesulfonyl chloride. The yield, boiling point or melting point and pertinent spectral data of these compounds are reported.展开更多
基金Natural Science Foundation of Shanghai,China(No.09ZR1401500)
文摘Poly[ 2, 2-（m.phenylene） -5, 5-bibenzimidazole] （mPBI） were synthesized by mixing 3, 3＇, 4, 4＇-tetraaminobiphenyl and isophthallc acid in 1 -butyl-3 -methyUmidazolinm chloride （ E BMIM] CI）. Intrinsic viscosity of mPBI polymers was 0.67 dL/g which was measured in 96% sulfuric acid. The polymer was characterized by Fourier transform infrared spectroscopy （FTIR）, nuclear magnetic resonance （ 1H-NMR ）, and thermogravimetric analysis （TGA）. The effects of polymerization conditions on the intrinsic viscosity of mPBI were investigated. It showed that the molecular weight of polymer mainly depended on pre-reaction time and reaction temperature. Comparison of structure and properties of mPBI synthesized in ionic liquids（ILs） and polyphosphoric acid was also reported. It indicates that the ionic liquids are a kind of good solvents in synthesis process of m_PBI and ionic liquids mainly affect molecular weight of mPBL
基金supported by the National Natural Science Foundation of China, No. 81160157projects of Science and Technology Bureau of Guizhou Province, No.20093075, 20072127
文摘Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2＇-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor.
文摘Aim Angiotensin II （AngII） induces vascular smooth muscle cell （VSMC） migration and growth, which is responsible for vascular remodeling during some cardiovascular diseases. It has been demonstrated to activate a C1 current, but the underlying mechanism is not clear. Methods Whole-cell patch clamp, co-immunoprecipitation （co-IP）, site-specific mutagenesis, angiotensinII-infusion hypertensive mice model were used. Results In VSMCs, AngII could induce a C1C-3-dependent C1- current that was abolished in C1C-3 null mice. The activation mechanism of this AngII-induced C1- current was ascribed to the interaction between C1C-3 and Rho-kinase 2 （ROCIL2）, as re- vealed by N-terminal or C-terminal truncation of C1C-3, ROCIC2 siRNA and Co-IP experiments. Then we searched for and identified the phosphorylation site of C1C-3 at threonine 532 is critical for AngII-induced C1- current and VSMC migration through ROCK. The C1C-3 T532D mutant （mutation of threonine 532 to aspartate）, mimicking the phos- phorylation state of C1C-3, significantly potentiated AngII-induced C1- current and VSMC migration; while C1C-3 T532A （mutation of threonine 532 to alanine） had the opposite effects. Furthermore, we found a remarkably de- creased AngII-induced VSMC migration in C1C-3 null mice that is insensitive to Y27632, an inhibitor of ROCIL2. In addition, AngII-induced cerebrovascular remodeling was ameliorated in C1C-3 null mice, possibly by ROCIL2 path- way. Conclusions C1C-3 protein phosphorylation at threonine 532 by ROCIL2 is required for AngII-induced C1- cur- rent and VSMC migration that are involved in AngII-induced hypertensive vascular remodeling.
基金The Project Supported by the National Science Foundation of U.S.A.
文摘1,1,1,-Trifluoro-2- substituted- phenyl- 2- propanols- 3- 14C were prepared from addition of methyl- 14C magnesium iodide to appropriate trifluoroacetophenone. These alcohols were converted into tosylatcs by reaction with n-butyllithium and then with p-toluenesulfonyl chloride. The yield, boiling point or melting point and pertinent spectral data of these compounds are reported.
