Journal: Journal of Clinical and Translational Hepatology

Article Title: Gasdermin D Inhibitor Necrosulfonamide Alleviates Lipopolysaccharide/D-galactosamine-induced Acute Liver Failure in Mice

doi: 10.14218/JCTH.2021.00560

Figure Lengend Snippet: Data are means±standard deviations (ALT, n=3; IL-1β and IL-18, n=5). ** p <0.01, *** p <0.001, **** p <0.0001. ALF, acute liver failure; ALT, alanine aminotransferase; D-GalN, D-galactosamine; DMSO, dimethyl sulfoxide; IL-1β, interleukin 1 beta; IL-18, interleukin 18; LPS, lipopolysaccharide; NSA, necrosulfonamide intervention group.

Article Snippet: Mice were randomly assigned to four groups using a random number table: (1) A normal control group ( n =10) with intraperitoneal injection of the same volume of saline as the ALF model modeling reagent; (2) An ALF group ( n =20) with intraperitoneal injection of LPS (Sigma-Aldrich, Saint Louis, Missouri, USA ) 50 µg/kg + D-GalN 800 mg/kg (Macklin, Shanghai, China) to establish an ALF model , ; (3) A dimethyl sulfoxide (DMSO) intervention group ( n =20) with intraperitoneal injection of the same amount of DMSO (Sigma-Aldrich) as the NSA group prior to establishment of the model; and (4) an NSA intervention group ( n =20) with NSA (EMD Millipore, Darmstadt, Germany ) dissolved in DMSO.

Techniques:

Journal: Biochemistry and Biophysics Reports

Article Title: Alleviation of lipopolysaccharide/ d -galactosamine-induced liver injury in leukocyte cell-derived chemotaxin 2 deficient mice

doi: 10.1016/j.bbrep.2017.09.011

Figure Lengend Snippet: The lower susceptibility of LECT2-deficient mice to LPS/ d -GalN acute liver injury. A mixture of d -GalN (700 mg/kg) and LPS (50 µg/kg) was intraperitoneally injected into wild-type (+/+) and LECT2-deficient (−/−) mice. (A) Comparison of survival rates between the wild-type ( n = 13) and LECT2-deficient ( n = 12) mice after injection with LPS/ d -GalN. The survival curves were created following the Kaplan–Meier method and compared by the log-rank (Mantel–Cox) test. The LECT2-deficient mice showed a significantly higher survival rate than the wild-type mice ( p < 0.001). (B) Serum GPT levels of wild-type and LECT2-deficient mice at 5 h after the injection of LPS/ d -GalN. Values are the mean and SEM of the results from six female mice. * p < 0.05. (C) Histopathological characterization of wild-type and LECT2-deficient mice at 5 h after the injection of LPS/ d -GalN. H&E stain at 200× magnification.

Article Snippet: Wild-type and LECT2-deficient mice were injected intraperitoneally with 700 mg/kg d -GalN (Nacalai Tesque, Kyoto, Japan) plus 50 μg/kg LPS (from Escherichia coli O111:B4; Sigma, St. Louis, MO).

Techniques: Injection, Comparison, Staining

Journal: Biochemistry and Biophysics Reports

Article Title: Alleviation of lipopolysaccharide/ d -galactosamine-induced liver injury in leukocyte cell-derived chemotaxin 2 deficient mice

doi: 10.1016/j.bbrep.2017.09.011

Figure Lengend Snippet: Serum levels and transcriptional levels of proinflammatory cytokines after LPS/ d -GalN administration. The serum levels of cytokines in wild-type (+/+) and LECT2-deficient (−/−) mice at 1.5 h (A) and 5 h (B) after the LPS/ d -GalN injection. Values are the mean and SEM of the results from 7 to 10 female mice. (C) Liver RNAs were prepared from mice at 1.5 h after LPS/ d -GalN administration. Quantitative real-time PCR was performed. The relative ratios of the PCR products in the wild-type ( n = 10) vs. the LECT2-deficient ( n = 8) mice are shown. * p < 0.05.

Article Snippet: Wild-type and LECT2-deficient mice were injected intraperitoneally with 700 mg/kg d -GalN (Nacalai Tesque, Kyoto, Japan) plus 50 μg/kg LPS (from Escherichia coli O111:B4; Sigma, St. Louis, MO).

Techniques: Injection, Real-time Polymerase Chain Reaction

Journal: Biochemistry and Biophysics Reports

Article Title: Alleviation of lipopolysaccharide/ d -galactosamine-induced liver injury in leukocyte cell-derived chemotaxin 2 deficient mice

doi: 10.1016/j.bbrep.2017.09.011

Figure Lengend Snippet: The reduction of IFN-γ-producing hepatic NK and NKT cells in the LECT2-deficient mice. (A) The numbers of NKT and NK cells in the livers of the wild-type (+/+) and the LECT2-deficient (−/−) mice on a BALB/c background were comparable. Two-color staining was performed for CD3 and CD49b (DX5), CD3 and CD1d-tetramer, and Mac-1 and Gr-1 against hepatic mononuclear cells. Representative flow cytometric plots are shown. (B–D) The IFN-γ-producing hepatic NK and NKT cells were reduced in the LECT2-deficient mice treated with LPS/ d -GalN. (B) Two-color staining for DX5 and IFN-γ against hepatic mononuclear cells in the wild-type (+/+) and LECT2-deficient (−/−) mice. (C) Detection of IFN-γ in DX5 + CD3 − NK cells by three-color staining for DX5, CD3, and IFN-γ. * p < 0.05. (D) Detection of IFN-γ in DX5 + CD3 + NKT cells. The numbers in the small panels of flow cytometric plots indicate the mean percentages and SEM of fluorescence-positive cells in the corresponding areas. Values are the mean and SEM of the results from 3 to 4 female mice.

Article Snippet: Wild-type and LECT2-deficient mice were injected intraperitoneally with 700 mg/kg d -GalN (Nacalai Tesque, Kyoto, Japan) plus 50 μg/kg LPS (from Escherichia coli O111:B4; Sigma, St. Louis, MO).

Techniques: Staining, Fluorescence