Journal: Scientific Reports

Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

doi: 10.1038/s41598-025-34506-1

Figure Lengend Snippet: rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 and TNF-α were detected via ELISA. ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).

Article Snippet: Supernatants collected from HTR-8/SVneo cells were assayed for IL-1β, IL-6, and TNF-α levels using a human ELISA kit (LiankeBio, Hangzhou, China).

Techniques: Activation Assay, Control, Enzyme-linked Immunosorbent Assay, Membrane, Expressing, Quantitative RT-PCR, Western Blot

Journal: Scientific Reports

Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

doi: 10.1038/s41598-025-34506-1

Figure Lengend Snippet: IL-37 knockdown enhances LPS-induced inflammatory and NLRP3 inflammasome activation in HTR-8/Svneo cells. ( A ) Cell supernatants were collected from control, si_NC- or si_IL37-treated cells following LPS exposure, and IL-37 expression level were detected by ELISA, qRT-PCR and Western blotting. ( B ) IL-1β, IL-6 and TNF-α levels in the cell supernatants were detected by ELISA. ( C ) The mRNA expression levels of NLRP3, Caspase-1 and ASC after cell treatment with LPS ( n = 5) were measured by qRT-PCR analysis. ( D ) NLRP3,pro-caspase-1, caspase-1 and ASC protein levels were detected by Western blotting, and the results were normalised to β-actin. All data exhibited equal variance.The data are shown as the mean ± s.e.m. The results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (One-way ANOVA).

Article Snippet: Supernatants collected from HTR-8/SVneo cells were assayed for IL-1β, IL-6, and TNF-α levels using a human ELISA kit (LiankeBio, Hangzhou, China).

Techniques: Knockdown, Activation Assay, Control, Expressing, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot

Journal: Scientific Reports

Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

doi: 10.1038/s41598-025-34506-1

Figure Lengend Snippet: Nigericin reversed the anti-inflammatory effects and effects of rhIL-37 and its inhibition of NF-κB p65 activation in LPS-induced PTB.t ( A ) Cell supernatants were collected from HTR-8/Svneo cells co-treated with rhIL-37 and LPS, then either left untreated or treated with nigericin.The mRNA expression of NLRP3, caspase-1, and ASC was detected. ( B ) Cells were collected, and the protein expression of NLRP3, caspase-1, pro-caspase-1, and ASC was detected by western blotting. Results were normalised to β-actin and statistically analyzed.( C ) HTR-8/Svneo cell supernatants were collected after co-treatment with rhIL-37 and LPS (with or without nigericin), and the expression levels of IL-1β, IL-6, and TNF-α were detected by ELISA. ( D ) HTR-8/Svneo cells co-treated with rhIL-37 and LPS (with or without nigericin) were collected. The mRNA expression of p65 was detected by qRT-PCR, and protein expression of p65 and p-p65 was detected by western blotting. Densitometric quantification of p-p65 relative to p65 was performed. Statistical analysis of the western blot results was performed.All data exhibited equal variance.The data are shown as the means ± s.e.m. The results are representative of at least three independent experiments..

Article Snippet: Supernatants collected from HTR-8/SVneo cells were assayed for IL-1β, IL-6, and TNF-α levels using a human ELISA kit (LiankeBio, Hangzhou, China).

Techniques: Inhibition, Activation Assay, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

Journal: Scientific Reports

Article Title: DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway

doi: 10.1038/s41598-026-42992-0

Figure Lengend Snippet: DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: Serum TNF-α levels were ascertained through an ELISA kit (E-MSEL-M0002, Elabscience Biotechnology Inc., Wuhan, China).

Techniques: Over Expression, Infection, Electron Microscopy, Staining, Injection, Phospho-proteomics