The new dithiocarbamate 4-vinylbenzyl 9H-carbazole-9-carbodithioate was synthesized and characterized by means of 1H NMR,elemental analysis,FT-IR,and X-ray crystallography.The crystal structure is of triclinic,space g...The new dithiocarbamate 4-vinylbenzyl 9H-carbazole-9-carbodithioate was synthesized and characterized by means of 1H NMR,elemental analysis,FT-IR,and X-ray crystallography.The crystal structure is of triclinic,space group Pī,with a=9.4301(19) nm,b=9.518(2) nm,c=10.541(2),α=83.909(16) °,β=77.279(13)°,γ=79.312(14) °,V=904.8(3) nm3,Z=2,F(000)=376,Dc=1.319 mg/ m3,final R1=0.0731,wR2=0.1615 for 10164 observed reflections with I> 2σ(I).The thermal stability of the title compound was also studied.The main released gas product of the thermal decomposition of the title compound were possibly nitrogen,carbon sulfide and hydrogen sulfide,and the final solid product was 14.5% carbon leavings.展开更多
AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of T...AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand Z-DVED-FMK.Cell viability was measured by CCK-8 assay.Annexin V/propidium iodide staining was used to count the number of apoptotic cells.DCFH-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow cytometry.The expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western blot.RESULTS:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger NAC.Moreover,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.展开更多
文摘The new dithiocarbamate 4-vinylbenzyl 9H-carbazole-9-carbodithioate was synthesized and characterized by means of 1H NMR,elemental analysis,FT-IR,and X-ray crystallography.The crystal structure is of triclinic,space group Pī,with a=9.4301(19) nm,b=9.518(2) nm,c=10.541(2),α=83.909(16) °,β=77.279(13)°,γ=79.312(14) °,V=904.8(3) nm3,Z=2,F(000)=376,Dc=1.319 mg/ m3,final R1=0.0731,wR2=0.1615 for 10164 observed reflections with I> 2σ(I).The thermal stability of the title compound was also studied.The main released gas product of the thermal decomposition of the title compound were possibly nitrogen,carbon sulfide and hydrogen sulfide,and the final solid product was 14.5% carbon leavings.
基金Supported by the National Natural Science Foundation of China(No.81172824)。
文摘AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand Z-DVED-FMK.Cell viability was measured by CCK-8 assay.Annexin V/propidium iodide staining was used to count the number of apoptotic cells.DCFH-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow cytometry.The expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western blot.RESULTS:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger NAC.Moreover,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.
