Acrylonitrile/N-[4-（aminosulfonyl）phenyl]acrylamide （AN/ASPAA） copolymers were synthesized and used as a host of lithium ion conducting electrolytes. The composition, molecular weight and molecular weight distribu...Acrylonitrile/N-[4-（aminosulfonyl）phenyl]acrylamide （AN/ASPAA） copolymers were synthesized and used as a host of lithium ion conducting electrolytes. The composition, molecular weight and molecular weight distribution of AN/ASPAA copolymers were determined, and the influence of copolymer composition on the glass temperature of AN/ASPAA copolymers and the ion conductivity of electrolytes were investigated. The molecular weights of AN/ASPAA copolymers were lower than those of AN and ASPAA homopolymers due to the cross-termination reaction. The glass temperatures of AN/ASPAA copolymers increased as the molar fraction of ASPAA units in copolymers increased. The lithium ion conductivities of the polymer electrolytes increased initially as the molar fraction of ASPAA units in copolymers increased, and a maximum conductivity was achieved when the molar fraction of ASPAA in the copolymer was 16.8%.展开更多
Drastic surges in intracellular reactive oxygen species(ROS)induce cell apoptosis,while most chemotherapy drugs lead to the accumulation of ROS.Here,we constructed an organic compound,arsenical N-(4-(1,3,2-dithiarsina...Drastic surges in intracellular reactive oxygen species(ROS)induce cell apoptosis,while most chemotherapy drugs lead to the accumulation of ROS.Here,we constructed an organic compound,arsenical N-(4-(1,3,2-dithiarsinan-2-yl)phenyl)acrylamide(AAZ2),which could prompt the ROS to trigger mitochondrial-dependent apoptosis in gastric cancer(GC).Mechanistically,by targeting pyruvate dehydrogenase kinase 1(PDK1),AAZ2 caused metabolism alteration and the imbalance of redox homeostasis,followed by the inhibition of phosphoinositide-3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway and leading to the activation of B-cell lymphoma 2(Bcl2)/Bcl2-associated X(Bax)/caspase-9(Cas9)/Cas3 cascades.Importantly,our in vivo data demonstrated that AAZ2 could inhibit the growth of GC xenograft.Overall,our data suggested that AAZ2 could contribute to metabolic abnormalities,leading to mitochondrial-dependent apoptosis by targeting PDK1 in GC.展开更多
文摘Acrylonitrile/N-[4-（aminosulfonyl）phenyl]acrylamide （AN/ASPAA） copolymers were synthesized and used as a host of lithium ion conducting electrolytes. The composition, molecular weight and molecular weight distribution of AN/ASPAA copolymers were determined, and the influence of copolymer composition on the glass temperature of AN/ASPAA copolymers and the ion conductivity of electrolytes were investigated. The molecular weights of AN/ASPAA copolymers were lower than those of AN and ASPAA homopolymers due to the cross-termination reaction. The glass temperatures of AN/ASPAA copolymers increased as the molar fraction of ASPAA units in copolymers increased. The lithium ion conductivities of the polymer electrolytes increased initially as the molar fraction of ASPAA units in copolymers increased, and a maximum conductivity was achieved when the molar fraction of ASPAA in the copolymer was 16.8%.
基金supported by the Wuhan University Zhongnan Hospital Translational Medicine and Interdisciplinary Research Joint Fund(No.ZNJC201910),China.
文摘Drastic surges in intracellular reactive oxygen species(ROS)induce cell apoptosis,while most chemotherapy drugs lead to the accumulation of ROS.Here,we constructed an organic compound,arsenical N-(4-(1,3,2-dithiarsinan-2-yl)phenyl)acrylamide(AAZ2),which could prompt the ROS to trigger mitochondrial-dependent apoptosis in gastric cancer(GC).Mechanistically,by targeting pyruvate dehydrogenase kinase 1(PDK1),AAZ2 caused metabolism alteration and the imbalance of redox homeostasis,followed by the inhibition of phosphoinositide-3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway and leading to the activation of B-cell lymphoma 2(Bcl2)/Bcl2-associated X(Bax)/caspase-9(Cas9)/Cas3 cascades.Importantly,our in vivo data demonstrated that AAZ2 could inhibit the growth of GC xenograft.Overall,our data suggested that AAZ2 could contribute to metabolic abnormalities,leading to mitochondrial-dependent apoptosis by targeting PDK1 in GC.
