AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal...AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal,and assessed by histological,serum transaminases,and mortality analyses. Hepatocellular apoptosis was quantified by transferase d UTP nick end labeling assay and Westernblot analysis of cleaved caspase-3. Liver inflammatory chemokine and cytochrome P450 expression was analyzed by quantitative reverse transcription-PCR. Neutrophil infiltration was evaluated by myeloperoxidase activity. Expression and phosphorylation of ERK,JNK,p65,and H2 A.X was determined by Western blot. Oxidative stress was evaluated by measuring malondialdehyde production and nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity.RESULTS: following LPS/D-Gal exposure,Recql5-deficient mice exhibited enhanced liver injury,as evidenced by more severe hepatic hemorrhage,higher serum aspartate transaminase and alanine transaminase levels,and lower survival rate. As compared to WT mice,Recql5-deficient mice showed an increased number of apoptotic hepatocytes and higher cleaved caspase-3 levels. Recql5-deficient mice exhibited increased DNA damage,as evidenced by increased γ-H2 A.X levels. Inflammatory cytokine levels,neutrophil infiltration,and ERK phosphorylation were also significantly increased in the knockout mice. Additionally,Recql5-deficicent mice exhibited increased malondialdehyde production and elevated inducible nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity,indicative of enhanced oxidative stress. Moreover,CYP450 expression was significantly downregulated in Recql5-deficient mice after LPS/D-Gal treatment.CONCLUSION: Recql5 protects the liver against LPS/D-Gal-induced injury through suppression of hepatocyte apoptosis and oxidative stress and modulation of CYP450 expression.展开更多
The oxidizing behavior of Si-containing steel was investigated in an O2 and N2 binary-component gas with oxygen contents ranging between 0.5 vol% and 4.0 vol% under anisothermal-oxidation conditions. A simultaneous th...The oxidizing behavior of Si-containing steel was investigated in an O2 and N2 binary-component gas with oxygen contents ranging between 0.5 vol% and 4.0 vol% under anisothermal-oxidation conditions. A simultaneous thermal analyzer was employed to simulate the heating process of Si-containing steel in industrial reheating furnaces. The oxidation gas mixtures were introduced from the commencement of heating. The results show that the oxidizing rate remains constant in the isothermal holding process at high temperatures; therefore, the mass change versus time presents a linear law. A linear relation also exists between the oxidizing rate and the oxygen content. Using the linear regression equation, the oxidation rate at different oxygen contents can be predicted. In addition, the relationship between the total mass gain and the oxygen content is linear; thus, the total mass gain at oxygen contents between 0.5 vol%–4.0 vol% can be determined. These results enrich the theoretical studies of the oxidation process in Si-containing steels.展开更多
基金Supported by National Natural Science Foundation of China,No.81101472 and No.81472556(to Liao W),and No.81372490(to Lu X)Zhejiang Provincial Natural Science Foundation,No.LZ14H160003(to Lu X)+2 种基金Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents(to Lu X)National Basic Research Program of China(973 Project),No.2011CB504603Wenzhou Municipal Science and Technology Bureau Foundation,No.Y20110090(to Li H)
文摘AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal,and assessed by histological,serum transaminases,and mortality analyses. Hepatocellular apoptosis was quantified by transferase d UTP nick end labeling assay and Westernblot analysis of cleaved caspase-3. Liver inflammatory chemokine and cytochrome P450 expression was analyzed by quantitative reverse transcription-PCR. Neutrophil infiltration was evaluated by myeloperoxidase activity. Expression and phosphorylation of ERK,JNK,p65,and H2 A.X was determined by Western blot. Oxidative stress was evaluated by measuring malondialdehyde production and nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity.RESULTS: following LPS/D-Gal exposure,Recql5-deficient mice exhibited enhanced liver injury,as evidenced by more severe hepatic hemorrhage,higher serum aspartate transaminase and alanine transaminase levels,and lower survival rate. As compared to WT mice,Recql5-deficient mice showed an increased number of apoptotic hepatocytes and higher cleaved caspase-3 levels. Recql5-deficient mice exhibited increased DNA damage,as evidenced by increased γ-H2 A.X levels. Inflammatory cytokine levels,neutrophil infiltration,and ERK phosphorylation were also significantly increased in the knockout mice. Additionally,Recql5-deficicent mice exhibited increased malondialdehyde production and elevated inducible nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity,indicative of enhanced oxidative stress. Moreover,CYP450 expression was significantly downregulated in Recql5-deficient mice after LPS/D-Gal treatment.CONCLUSION: Recql5 protects the liver against LPS/D-Gal-induced injury through suppression of hepatocyte apoptosis and oxidative stress and modulation of CYP450 expression.
基金financially supported by the National Natural Science Foundation of China(No.51274154)The Major Projects of Technology Innovation of Hubei Province,China(No.2017AAA116)the Special Fund of Wuhan University of Science and Technology for Master Student’s Short-Term Studying Abroad
文摘The oxidizing behavior of Si-containing steel was investigated in an O2 and N2 binary-component gas with oxygen contents ranging between 0.5 vol% and 4.0 vol% under anisothermal-oxidation conditions. A simultaneous thermal analyzer was employed to simulate the heating process of Si-containing steel in industrial reheating furnaces. The oxidation gas mixtures were introduced from the commencement of heating. The results show that the oxidizing rate remains constant in the isothermal holding process at high temperatures; therefore, the mass change versus time presents a linear law. A linear relation also exists between the oxidizing rate and the oxygen content. Using the linear regression equation, the oxidation rate at different oxygen contents can be predicted. In addition, the relationship between the total mass gain and the oxygen content is linear; thus, the total mass gain at oxygen contents between 0.5 vol%–4.0 vol% can be determined. These results enrich the theoretical studies of the oxidation process in Si-containing steels.
