Drought stress is a devastating natural disaster driven by the continuing intensification of global warming,which seriously threatens the productivity and quality of several horticultural crops,including pear.Gibberel...Drought stress is a devastating natural disaster driven by the continuing intensification of global warming,which seriously threatens the productivity and quality of several horticultural crops,including pear.Gibberellins(GAs)play crucial roles in plant growth,development,and responses to drought stress.Previous studies have shown significant reductions of GA levels in plants under drought stress;however,our understanding of the intrinsic regulation mechanisms of GA-mediated drought stress in pear remains very limited.Here,we show that drought stress can impair the accumulation of bioactive GAs(BGAs),and subsequently identified PbrGA2ox1 as a chloroplast-localized GA deactivation gene.This gene was significantly induced by drought stress and abscisic acid(ABA)treatment,but was suppressed by GA_(3)treatment.PbrGA2ox1-overexpressing transgenic tobacco plants(Nicotiana benthamiana)exhibited enhanced tolerance to dehydration and drought stresses,whereas knock-down of PbrGA2ox1 in pear(Pyrus betulaefolia)by virus-induced gene silencing led to elevated drought sensitivity.Transgenic plants were hypersensitive to ABA,and had a lower BGAs content,enhanced reactive oxygen species(ROS)scavenging ability,and augmented ABA accumulation and signaling under drought stress compared to wild-type plants.However,the opposite effects were observed with PbrGA2ox1 silencing in pear.Moreover,exogenous GA_(3)treatment aggravated the ROS toxic effect and restrained ABA synthesis and signaling,resulting in the compromised drought tolerance of pear.In summary,our results shed light on the mechanism by which BGAs are eliminated in pear leaves under drought stress,providing further insights into the mechanism regulating the effects of GA on the drought tolerance of plants.展开更多
Objective: To evaluate the anti-tumor effects of SeO2 and its mechanisms on three human lung cancer cell lines. Methods: Three lung cancer cells A549, GLC-82 and PG were treated with 3-30 μmol/L SeO2. Flow cytometry ...Objective: To evaluate the anti-tumor effects of SeO2 and its mechanisms on three human lung cancer cell lines. Methods: Three lung cancer cells A549, GLC-82 and PG were treated with 3-30 μmol/L SeO2. Flow cytometry was used to detect apoptosis, and analyze the changes of expression of p53 and Bcl-2, as well as ROS and Ca2+ level within cells. Results:SeO2 markedly inhibited cell proliferation and viability, and prompted apoptosis after 48 h treatment. SeO2 at 10 μmol/L induced 47.8% apoptosis in A549 cells, 40.8% in GLC-82 cells, 18.2% in PG cells. SeO2 at 30 μmol/L induced 37.8% apoposis in PG cells,but did not increase apoptotic raes in other two cells. SeO2 could down-regulate the mean fluorescent intensity of Bcl-2 from 65.8 to 9.6 in A549, but not in GLC-82 and in PG cells, up-regulate wild type p53 level in all three cells. SeO2 decreased the ROS and Ca2+ level markedly within three tested cells. Conclusion: SeO2 showed anti-tumor effect via apoptosis pathway in three lung cancer cell lines. The decrease of ROS and Ca2+ level within cells as well as regulation of Bcl-2 and p53 expression may play important roles in above apoptotic procedure.展开更多
Titania (TiO2) induced photocatalysis has been widely investigated and applied as a disinfection strategy in many industrial and clinical applications. Reactive oxygen species (ROS), including hydroxyl radicals (&...Titania (TiO2) induced photocatalysis has been widely investigated and applied as a disinfection strategy in many industrial and clinical applications. Reactive oxygen species (ROS), including hydroxyl radicals (&8226OH), superoxide radicals () and hydrogen peroxide (H2O2), generated in the photocatalytic reaction process are considered to be the active components prompting the bactericidal effect. In the present work, the kinetics of photocatalytic inactivation of Staphylococcus epidermidis and specific contributions of •OH, and H2O2 to the bactericidal process were studied using two disinfection settings sutilizing photocatalytic resin-TiO2 nanocomposite surfaces and suspended TiO2 nanoparticles, respectively. In antibacterial tests against S. epidermidis with a layer of bacterial suspension on the resin-TiO2 surfaces, H2O2 was found to be the most efficient ROS component contributing to the antibacterial effect. Disinfection kinetics showed a two-step behavior with an initial region having a lower disinfection rate followed by a higher rate region after 10 min of UV irradiation. By contrast, in antibacterial tests with suspended bacteria and photocatalytic TiO2 nanoparticles, •OH and H2O2 showed equal significance in the bacterial inactivation having a typical Chick-Watson disinfection kinetics behavior with a steady disinfection rate. The results contribute to the understanding of the bactericidal mechanism and kinetics of photocatalytic disinfection that are essential for designing specific antibacterial applications of photocatalytic materials.展开更多
It is urgent to develop catalysts with application potential for oxidative coupling of methane(OCM)at relatively lower temperature.Herein,three-dimensional ordered macro porous(3 DOM)La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)(...It is urgent to develop catalysts with application potential for oxidative coupling of methane(OCM)at relatively lower temperature.Herein,three-dimensional ordered macro porous(3 DOM)La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)(A_(2)B_(2)O_(7)-type)catalysts with disordered defective cubic fluorite phased structure were successfully prepared by a colloidal crystal template method.3DOM structure promotes the accessibility of the gaseous reactants(O2and CH4)to the active sites.The co-doping of Ca and Sr ions in La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts improved the formation of oxygen vacancies,thereby leading to increased density of surface-active oxygen species(O_(2)^(-))for the activation of CH4and the formation of C2products(C2H6and C2H4).3DOM La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts exhibit high catalytic activity for OCM at low temperature.3DOM La1.7Sr0.3Ce1.7Ca0.3O7-δcatalyst with the highest density of O_(2)^(-)species exhibited the highest catalytic activity for low-temperature OCM,i.e.,its CH4conversion,selectivity and yield of C2products at 650℃are 32.2%,66.1%and 21.3%,respectively.The mechanism was proposed that the increase in surface oxygen vacancies induced by the co-doping of Ca and Sr ions boosts the key step of C-H bond breaking and C-C bond coupling in catalyzing low-temperature OCM.It is meaningful for the development of the low-temperature and high-efficient catalysts for OCM reaction in practical application.展开更多
Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of N...Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.展开更多
Vanadium oxide cathode materials with stable crystal structure and fast Zn^(2+) storage capabilities are extremely important to achieving outstanding electrochemical performance in aqueous zinc‐ion batteries.In this ...Vanadium oxide cathode materials with stable crystal structure and fast Zn^(2+) storage capabilities are extremely important to achieving outstanding electrochemical performance in aqueous zinc‐ion batteries.In this work,a one‐step hydrothermal method was used to manipulate the bimetallic ion intercalation into the interlayer of vanadium oxide.The pre‐intercalated Cu ions act as pillars to pin the vanadium oxide(V‐O)layers,establishing stabilized two‐dimensional channels for fast Zn^(2+) diffusion.The occupation of Mn ions between V‐O interlayer further expands the layer spacing and increases the concentration of oxygen defects(Od),which boosts the Zn^(2+) diffusion kinetics.As a result,as‐prepared Cu_(0.17)Mn_(0.03)V_(2)O_(5−□)·2.16H_(2)O cathode shows outstanding Zn‐storage capabilities under room‐and lowtemperature environments(e.g.,440.3 mAh g^(−1) at room temperature and 294.3 mAh g^(−1)at−60°C).Importantly,it shows a long cycling life and high capacity retention of 93.4%over 2500 cycles at 2 A g^(−1) at−60°C.Furthermore,the reversible intercalation chemistry mechanisms during discharging/charging processes were revealed via operando X‐ray powder diffraction and ex situ Raman characterizations.The strategy of a couple of 3d transition metal doping provides a solution for the development of superior room‐/lowtemperature vanadium‐based cathode materials.展开更多
AIM: To investigated the effects of urotensin Ⅱ(UII) on hepatic insulin resistance in Hep G2 cells and the potential mechanisms involved.METHODS: Human hepatoma Hep G2 cells were cultured with or without exogenous UI...AIM: To investigated the effects of urotensin Ⅱ(UII) on hepatic insulin resistance in Hep G2 cells and the potential mechanisms involved.METHODS: Human hepatoma Hep G2 cells were cultured with or without exogenous UII for 24 h, in the presence or absence of 100 nmol/L insulin for the last 30 min. Glucose levels were detected by the glucoseoxidase method and glycogen synthesis was analyzed by glycogen colorimetric/fluorometric assay. Reactive oxygen species(ROS) levels were detected with a multimode reader using a 2′,7′-dichlorofluorescein diacetate probe. The protein expression and phosphorylation levels of c-Jun N-terminal kinase(JNK), insulin signal essential molecules such as insulin receptor substrate-1(IRS-1), protein kinase B(Akt), glycogen synthase kinase-3β(GSK-3β), and glucose transporter-2(Glut 2), and NADPH oxidase subunits such as gp91 phox, p67 phox, p47 phox, p40 phox, and p22 phox were evaluated by Western blot.RESULTS: Exposure to 100 nmol/L UII reduced the insulin-induced glucose consumption(P < 0.05)and glycogen content(P < 0.01) in Hep G2 cells compared with cells without UII. UII also abolished insulin-stimulated protein expression(P < 0.01) and phosphorylation of IRS-1(P < 0.05), associated with down-regulation of Akt(P < 0.05) and GSK-3β(P < 0.05) phosphorylation levels, and the expression of Glut 2(P < 0.001), indicating an insulin-resistance state in Hep G2 cells. Furthermore, UII enhanced the phosphorylation of JNK(P < 0.05), while the activity of JNK, insulin signaling, such as total protein of IRS-1(P < 0.001), phosphorylation of IRS-1(P < 0.001) and GSK-3β(P < 0.05), and glycogen synthesis(P < 0.001) could be reversed by pretreatment with the JNK inhibitor SP600125. Besides, UII markedly improved ROS generation(P < 0.05) and NADPH oxidase subunit expression(P < 0.05). However, the antioxidant/NADPH oxidase inhibitor apocynin could decrease UII-induced ROS production(P < 0.05), JNK phosphorylation(P < 0.05), and insulin resistance(P < 0.05) in HepG 2 cells. CONCLUSION: UII induces insulin resistance, and this can be reversed by JNK inhibitor SP600125 and antioxidant/NADPH oxidase inhibitor apocynin targeting the insulin signaling pathway in HepG 2 cells.展开更多
AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture,...AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Lucigenin assay showed the generation of ROS in cells under incubation with JTE-522. The increased ROS generation might contribute to the induction of AGS cells to apoptosis. EMSA and Western blot revealed that NF-kB activity was almost completely inhibited by preventing the degradation of IkBalpha. Additionally, by using Western blot we confirmed that the level of bcl-2 was decreased, whereas p53 showed a great increase following JTE-522 treatment. Their changes were in a dose-dependent manner. CONCLUSION: These findings suggest that reactive oxygen species, NF-kB, p53, bcl-2 and caspase-3 may play an important role in the induction of apoptosis in AGS cells after treatment with JTE-522.展开更多
The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension,preeclampsia,and renal-allograft rejection,but the detailed mechanisms remain unclear.In order...The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension,preeclampsia,and renal-allograft rejection,but the detailed mechanisms remain unclear.In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide,15 mice were divided into three groups:control group,AT1-EC2-immunized group,and AT1-EC2-immunized and valsartan-treated group.In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times:0,5,10,and 15 days after the experiment.In AT1-EC2-immunized and valsartan-treated group,valsartan was given at a dose of 100 mg/kg every day for 20 days.After the experiment,the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments.The titer of AT1-EC2 was assayed by using ELISA.The level of NOX1 mRNA in the aorta was determined by using RT-PCR.The expression of NOX1 was detected by using Western blotting.Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue.The O 2.production was detected in situ after DHE staining.The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group.There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group.The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group,and the O 2.production increased about 2.7 times as compared with control group.There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group.It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS,and increase vascular inflammation,which can be inhibited by AT1 receptor blocker valsartan.This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.展开更多
AIM:To investigate the role of reactive oxygen species(ROS)in epithelial–mesenchymal transition(EMT)and apoptosis of human lens epithelial cells(HLECs).METHODS:Flow cytometry was used to assess ROS production after t...AIM:To investigate the role of reactive oxygen species(ROS)in epithelial–mesenchymal transition(EMT)and apoptosis of human lens epithelial cells(HLECs).METHODS:Flow cytometry was used to assess ROS production after transforming growth factorβ2(TGF-β2)induction.Apoptosis of HLECs after H_(2)O_(2) and TGF-β2 interference with or without ROS scavenger N-acetylcysteine(NAC)were assessed by flow cytometry.The corresponding protein expression levels of the EMT markerα-smooth muscle actin(α-SMA),the extracellular matrix(ECM),marker fibronectin(Fn),and apoptosis-associated proteins were detected by using Western blotting in the presence of an ROS scavenger(NAC).Wound-healing and Transwell assays were used to assess the migration capability of HLECs.RESULTS:TGF-β2 stimulates ROS production within 8h in HLECs.Additionally,TGF-β2 induced HLECs cell apoptosis,EMT/ECM synthesis protein markers expression,and pro-apoptotic proteins production;nonetheless,NAC treatment prevented these responses.Similarly,TGF-β2 promoted HLECs cell migration,whereas NAC inhibited cell migration.We further determined that although ROS initiated apoptosis,it only induced the accumulation of the EMT markerα-SMA protein,but not COL-1 or Fn.CONCLUSION:ROS contribute to TGF-β2-induced EMT/ECM synthesis and cell apoptosis of HLECs;however,ROS alone are not sufficient for EMT/ECM synthesis.展开更多
Apoptosis of dopaminergic neurons in the nigrostriatal projection plays a crucial role in the pathogenesis of Parkinson’s disease (PD). Although the detailed mechanisms responsible for dopaminergic neuron loss are st...Apoptosis of dopaminergic neurons in the nigrostriatal projection plays a crucial role in the pathogenesis of Parkinson’s disease (PD). Although the detailed mechanisms responsible for dopaminergic neuron loss are still under investigation, oxidative stress is identified as a major contributor for neuronal apoptosis. In the current study, we studied the effects of MPP+, a substrate that mimics oxidative stress, on neuron-like PC12 cells and the underlying mechanisms. PC12 cells were cultured and treated by 100 μmol/L MPP+ for 4, 8, 16, 24 and 48 h, respectively. For drug pretreatment, the PC12 cells were incubated with N-acetyl-l-cysteine (NAC, 5 mmol/L), an antioxidant, SP600125 (20 μmol/L) or PD98059 (100 μmol/L), two pharmacological inhibitors of JNK and ERK1/2, for 1 h before addition of MPP+. Cell apoptosis was measured by flow cytometry. The mRNA expression of Cu2+/Zn2+-SOD, GSH-Px, Bcl-2 and Bax was detected by RT-PCR. The protein expression of p-ERK1/2 and p-JNK was determined by Western blotting. Our results showed that MPP+ exposure could induce substantial PC12 cell apoptosis. The pretreatment of SP600125 or PD98059 could effectively reduce the apoptosis rate by reducing the ratio of Bax/Bcl-2 mRNA levels. MPP+ exposure also induced high level of reactive oxy-gen species (ROS), marked by dramatic increase of Cu2+/Zn2+-SOD and GSH-Px mRNA levels. The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP+ exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Finally, the pretreatment of SP600125, but not PD98059, alleviated the increase of Cu2+/Zn2+-SOD and GSH-Px mRNAs induced by MPP+, suggesting that the activation of the JNK signal pathway, but not the ERK1/2 signal pathway, could, in some degree, antagonize the generation of ROS induced by oxidative stress. In conclusion, our results suggest that JNK and ERK1/2 signal pathways, which are activated via ROS, play a crucial role in neuronal apoptosis induced by oxidative stress.展开更多
基金supported by grants from the China Agriculture Research System(CARS-28-14)the Technical System of Fruit Industry in Anhui Province,China(AHCYTX-10)the Scientific Research Projects for Postgraduates of Anhui Universities,China(YJS20210207).
文摘Drought stress is a devastating natural disaster driven by the continuing intensification of global warming,which seriously threatens the productivity and quality of several horticultural crops,including pear.Gibberellins(GAs)play crucial roles in plant growth,development,and responses to drought stress.Previous studies have shown significant reductions of GA levels in plants under drought stress;however,our understanding of the intrinsic regulation mechanisms of GA-mediated drought stress in pear remains very limited.Here,we show that drought stress can impair the accumulation of bioactive GAs(BGAs),and subsequently identified PbrGA2ox1 as a chloroplast-localized GA deactivation gene.This gene was significantly induced by drought stress and abscisic acid(ABA)treatment,but was suppressed by GA_(3)treatment.PbrGA2ox1-overexpressing transgenic tobacco plants(Nicotiana benthamiana)exhibited enhanced tolerance to dehydration and drought stresses,whereas knock-down of PbrGA2ox1 in pear(Pyrus betulaefolia)by virus-induced gene silencing led to elevated drought sensitivity.Transgenic plants were hypersensitive to ABA,and had a lower BGAs content,enhanced reactive oxygen species(ROS)scavenging ability,and augmented ABA accumulation and signaling under drought stress compared to wild-type plants.However,the opposite effects were observed with PbrGA2ox1 silencing in pear.Moreover,exogenous GA_(3)treatment aggravated the ROS toxic effect and restrained ABA synthesis and signaling,resulting in the compromised drought tolerance of pear.In summary,our results shed light on the mechanism by which BGAs are eliminated in pear leaves under drought stress,providing further insights into the mechanism regulating the effects of GA on the drought tolerance of plants.
基金This project was partially supported by Science Foundation of Lanzhou Command of PLA(No.YZ-0106).
文摘Objective: To evaluate the anti-tumor effects of SeO2 and its mechanisms on three human lung cancer cell lines. Methods: Three lung cancer cells A549, GLC-82 and PG were treated with 3-30 μmol/L SeO2. Flow cytometry was used to detect apoptosis, and analyze the changes of expression of p53 and Bcl-2, as well as ROS and Ca2+ level within cells. Results:SeO2 markedly inhibited cell proliferation and viability, and prompted apoptosis after 48 h treatment. SeO2 at 10 μmol/L induced 47.8% apoptosis in A549 cells, 40.8% in GLC-82 cells, 18.2% in PG cells. SeO2 at 30 μmol/L induced 37.8% apoposis in PG cells,but did not increase apoptotic raes in other two cells. SeO2 could down-regulate the mean fluorescent intensity of Bcl-2 from 65.8 to 9.6 in A549, but not in GLC-82 and in PG cells, up-regulate wild type p53 level in all three cells. SeO2 decreased the ROS and Ca2+ level markedly within three tested cells. Conclusion: SeO2 showed anti-tumor effect via apoptosis pathway in three lung cancer cell lines. The decrease of ROS and Ca2+ level within cells as well as regulation of Bcl-2 and p53 expression may play important roles in above apoptotic procedure.
基金The Carl Trygger Foundation,The Goran Gustafsson Foundation,The Swedish Research Council,Vinnova and The Swedish Foundation for Strategic Research for financially supporting this work
文摘Titania (TiO2) induced photocatalysis has been widely investigated and applied as a disinfection strategy in many industrial and clinical applications. Reactive oxygen species (ROS), including hydroxyl radicals (&8226OH), superoxide radicals () and hydrogen peroxide (H2O2), generated in the photocatalytic reaction process are considered to be the active components prompting the bactericidal effect. In the present work, the kinetics of photocatalytic inactivation of Staphylococcus epidermidis and specific contributions of •OH, and H2O2 to the bactericidal process were studied using two disinfection settings sutilizing photocatalytic resin-TiO2 nanocomposite surfaces and suspended TiO2 nanoparticles, respectively. In antibacterial tests against S. epidermidis with a layer of bacterial suspension on the resin-TiO2 surfaces, H2O2 was found to be the most efficient ROS component contributing to the antibacterial effect. Disinfection kinetics showed a two-step behavior with an initial region having a lower disinfection rate followed by a higher rate region after 10 min of UV irradiation. By contrast, in antibacterial tests with suspended bacteria and photocatalytic TiO2 nanoparticles, •OH and H2O2 showed equal significance in the bacterial inactivation having a typical Chick-Watson disinfection kinetics behavior with a steady disinfection rate. The results contribute to the understanding of the bactericidal mechanism and kinetics of photocatalytic disinfection that are essential for designing specific antibacterial applications of photocatalytic materials.
基金supported by the National Key Research and Development Program of China(Nos.2022YFB3504100,2022YFB3506200)the National Natural Science Foundation of China(Nos.22208373,22376217)+1 种基金the Beijing Nova Program(No.20220484215)the Science Foundation of China University of Petroleum,Beijing(No.2462023YJRC030)。
文摘It is urgent to develop catalysts with application potential for oxidative coupling of methane(OCM)at relatively lower temperature.Herein,three-dimensional ordered macro porous(3 DOM)La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)(A_(2)B_(2)O_(7)-type)catalysts with disordered defective cubic fluorite phased structure were successfully prepared by a colloidal crystal template method.3DOM structure promotes the accessibility of the gaseous reactants(O2and CH4)to the active sites.The co-doping of Ca and Sr ions in La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts improved the formation of oxygen vacancies,thereby leading to increased density of surface-active oxygen species(O_(2)^(-))for the activation of CH4and the formation of C2products(C2H6and C2H4).3DOM La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts exhibit high catalytic activity for OCM at low temperature.3DOM La1.7Sr0.3Ce1.7Ca0.3O7-δcatalyst with the highest density of O_(2)^(-)species exhibited the highest catalytic activity for low-temperature OCM,i.e.,its CH4conversion,selectivity and yield of C2products at 650℃are 32.2%,66.1%and 21.3%,respectively.The mechanism was proposed that the increase in surface oxygen vacancies induced by the co-doping of Ca and Sr ions boosts the key step of C-H bond breaking and C-C bond coupling in catalyzing low-temperature OCM.It is meaningful for the development of the low-temperature and high-efficient catalysts for OCM reaction in practical application.
基金Supported by the Natural Science Foundation of Heilongjiang Province(LH2019C021)。
文摘Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.
基金National Natural Science Foundation of China,Grant/Award Numbers:52372188,51902090,51922008,520721142023 Introduction of studying abroad talent program,the China Postdoctoral Science Foundation,Grant/Award Number:2019 M652546+3 种基金Xinxiang Major Science and Technology Projects,Grant/Award Number:21ZD001Henan Province Postdoctoral Start‐Up Foundation,Grant/Award Number:1901017Henan Center for Outstanding Overseas Scientists,Grant/Award Number:GZS2018003Overseas Expertise Introduction Project for Discipline Innovation,Grant/Award Number:D17007。
文摘Vanadium oxide cathode materials with stable crystal structure and fast Zn^(2+) storage capabilities are extremely important to achieving outstanding electrochemical performance in aqueous zinc‐ion batteries.In this work,a one‐step hydrothermal method was used to manipulate the bimetallic ion intercalation into the interlayer of vanadium oxide.The pre‐intercalated Cu ions act as pillars to pin the vanadium oxide(V‐O)layers,establishing stabilized two‐dimensional channels for fast Zn^(2+) diffusion.The occupation of Mn ions between V‐O interlayer further expands the layer spacing and increases the concentration of oxygen defects(Od),which boosts the Zn^(2+) diffusion kinetics.As a result,as‐prepared Cu_(0.17)Mn_(0.03)V_(2)O_(5−□)·2.16H_(2)O cathode shows outstanding Zn‐storage capabilities under room‐and lowtemperature environments(e.g.,440.3 mAh g^(−1) at room temperature and 294.3 mAh g^(−1)at−60°C).Importantly,it shows a long cycling life and high capacity retention of 93.4%over 2500 cycles at 2 A g^(−1) at−60°C.Furthermore,the reversible intercalation chemistry mechanisms during discharging/charging processes were revealed via operando X‐ray powder diffraction and ex situ Raman characterizations.The strategy of a couple of 3d transition metal doping provides a solution for the development of superior room‐/lowtemperature vanadium‐based cathode materials.
基金Supported by National Natural Science Foundation of China,No.81272757the Project of Construction of Innovative Teams and Teacher Career Development for Universities and Colleges under Beijing Municipality,No.IDHT20150502
文摘AIM: To investigated the effects of urotensin Ⅱ(UII) on hepatic insulin resistance in Hep G2 cells and the potential mechanisms involved.METHODS: Human hepatoma Hep G2 cells were cultured with or without exogenous UII for 24 h, in the presence or absence of 100 nmol/L insulin for the last 30 min. Glucose levels were detected by the glucoseoxidase method and glycogen synthesis was analyzed by glycogen colorimetric/fluorometric assay. Reactive oxygen species(ROS) levels were detected with a multimode reader using a 2′,7′-dichlorofluorescein diacetate probe. The protein expression and phosphorylation levels of c-Jun N-terminal kinase(JNK), insulin signal essential molecules such as insulin receptor substrate-1(IRS-1), protein kinase B(Akt), glycogen synthase kinase-3β(GSK-3β), and glucose transporter-2(Glut 2), and NADPH oxidase subunits such as gp91 phox, p67 phox, p47 phox, p40 phox, and p22 phox were evaluated by Western blot.RESULTS: Exposure to 100 nmol/L UII reduced the insulin-induced glucose consumption(P < 0.05)and glycogen content(P < 0.01) in Hep G2 cells compared with cells without UII. UII also abolished insulin-stimulated protein expression(P < 0.01) and phosphorylation of IRS-1(P < 0.05), associated with down-regulation of Akt(P < 0.05) and GSK-3β(P < 0.05) phosphorylation levels, and the expression of Glut 2(P < 0.001), indicating an insulin-resistance state in Hep G2 cells. Furthermore, UII enhanced the phosphorylation of JNK(P < 0.05), while the activity of JNK, insulin signaling, such as total protein of IRS-1(P < 0.001), phosphorylation of IRS-1(P < 0.001) and GSK-3β(P < 0.05), and glycogen synthesis(P < 0.001) could be reversed by pretreatment with the JNK inhibitor SP600125. Besides, UII markedly improved ROS generation(P < 0.05) and NADPH oxidase subunit expression(P < 0.05). However, the antioxidant/NADPH oxidase inhibitor apocynin could decrease UII-induced ROS production(P < 0.05), JNK phosphorylation(P < 0.05), and insulin resistance(P < 0.05) in HepG 2 cells. CONCLUSION: UII induces insulin resistance, and this can be reversed by JNK inhibitor SP600125 and antioxidant/NADPH oxidase inhibitor apocynin targeting the insulin signaling pathway in HepG 2 cells.
基金National Natural Science Foundation of China,No.39770300,30070873the Overseas Chinese Affairs Office of the State Council Foundation,No.98-33
文摘AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Lucigenin assay showed the generation of ROS in cells under incubation with JTE-522. The increased ROS generation might contribute to the induction of AGS cells to apoptosis. EMSA and Western blot revealed that NF-kB activity was almost completely inhibited by preventing the degradation of IkBalpha. Additionally, by using Western blot we confirmed that the level of bcl-2 was decreased, whereas p53 showed a great increase following JTE-522 treatment. Their changes were in a dose-dependent manner. CONCLUSION: These findings suggest that reactive oxygen species, NF-kB, p53, bcl-2 and caspase-3 may play an important role in the induction of apoptosis in AGS cells after treatment with JTE-522.
基金supported by National Natural Science Foundation of China (No. 30871069)
文摘The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension,preeclampsia,and renal-allograft rejection,but the detailed mechanisms remain unclear.In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide,15 mice were divided into three groups:control group,AT1-EC2-immunized group,and AT1-EC2-immunized and valsartan-treated group.In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times:0,5,10,and 15 days after the experiment.In AT1-EC2-immunized and valsartan-treated group,valsartan was given at a dose of 100 mg/kg every day for 20 days.After the experiment,the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments.The titer of AT1-EC2 was assayed by using ELISA.The level of NOX1 mRNA in the aorta was determined by using RT-PCR.The expression of NOX1 was detected by using Western blotting.Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue.The O 2.production was detected in situ after DHE staining.The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group.There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group.The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group,and the O 2.production increased about 2.7 times as compared with control group.There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group.It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS,and increase vascular inflammation,which can be inhibited by AT1 receptor blocker valsartan.This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.
基金Supported by the National Natural Science Foundation of China(No.82201163,No.81800812)Natural Science Foundation Youth Foundation of Shaanxi Province(No.2023-JC-QN-0861)Shaanxi Province Key Research and Development Program(No.2023-YBSF-483).
文摘AIM:To investigate the role of reactive oxygen species(ROS)in epithelial–mesenchymal transition(EMT)and apoptosis of human lens epithelial cells(HLECs).METHODS:Flow cytometry was used to assess ROS production after transforming growth factorβ2(TGF-β2)induction.Apoptosis of HLECs after H_(2)O_(2) and TGF-β2 interference with or without ROS scavenger N-acetylcysteine(NAC)were assessed by flow cytometry.The corresponding protein expression levels of the EMT markerα-smooth muscle actin(α-SMA),the extracellular matrix(ECM),marker fibronectin(Fn),and apoptosis-associated proteins were detected by using Western blotting in the presence of an ROS scavenger(NAC).Wound-healing and Transwell assays were used to assess the migration capability of HLECs.RESULTS:TGF-β2 stimulates ROS production within 8h in HLECs.Additionally,TGF-β2 induced HLECs cell apoptosis,EMT/ECM synthesis protein markers expression,and pro-apoptotic proteins production;nonetheless,NAC treatment prevented these responses.Similarly,TGF-β2 promoted HLECs cell migration,whereas NAC inhibited cell migration.We further determined that although ROS initiated apoptosis,it only induced the accumulation of the EMT markerα-SMA protein,but not COL-1 or Fn.CONCLUSION:ROS contribute to TGF-β2-induced EMT/ECM synthesis and cell apoptosis of HLECs;however,ROS alone are not sufficient for EMT/ECM synthesis.
文摘Apoptosis of dopaminergic neurons in the nigrostriatal projection plays a crucial role in the pathogenesis of Parkinson’s disease (PD). Although the detailed mechanisms responsible for dopaminergic neuron loss are still under investigation, oxidative stress is identified as a major contributor for neuronal apoptosis. In the current study, we studied the effects of MPP+, a substrate that mimics oxidative stress, on neuron-like PC12 cells and the underlying mechanisms. PC12 cells were cultured and treated by 100 μmol/L MPP+ for 4, 8, 16, 24 and 48 h, respectively. For drug pretreatment, the PC12 cells were incubated with N-acetyl-l-cysteine (NAC, 5 mmol/L), an antioxidant, SP600125 (20 μmol/L) or PD98059 (100 μmol/L), two pharmacological inhibitors of JNK and ERK1/2, for 1 h before addition of MPP+. Cell apoptosis was measured by flow cytometry. The mRNA expression of Cu2+/Zn2+-SOD, GSH-Px, Bcl-2 and Bax was detected by RT-PCR. The protein expression of p-ERK1/2 and p-JNK was determined by Western blotting. Our results showed that MPP+ exposure could induce substantial PC12 cell apoptosis. The pretreatment of SP600125 or PD98059 could effectively reduce the apoptosis rate by reducing the ratio of Bax/Bcl-2 mRNA levels. MPP+ exposure also induced high level of reactive oxy-gen species (ROS), marked by dramatic increase of Cu2+/Zn2+-SOD and GSH-Px mRNA levels. The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP+ exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Finally, the pretreatment of SP600125, but not PD98059, alleviated the increase of Cu2+/Zn2+-SOD and GSH-Px mRNAs induced by MPP+, suggesting that the activation of the JNK signal pathway, but not the ERK1/2 signal pathway, could, in some degree, antagonize the generation of ROS induced by oxidative stress. In conclusion, our results suggest that JNK and ERK1/2 signal pathways, which are activated via ROS, play a crucial role in neuronal apoptosis induced by oxidative stress.
