il 18  (Proteintech)

Journal: PLOS One

Article Title: A new mechanism regulating microglial NLRP3 inflammasome: FMR1 mediates NLRP3 mRNA stability

doi: 10.1371/journal.pone.0341867

Figure Lengend Snippet: (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β and IL-18 in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.

Article Snippet: The levels of IL-1β and IL-18 in the supernatant of treated BV2 microglia were determined using Mouse IL-1β ELISA Kit (#EK201B) and Mouse IL-18 ELISA Kit (#EK218), respectively, as described by the vendor (Multi Sciences, Hangzhou, China).

Techniques: Western Blot, Control, Activity Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

Journal: PLOS One

Article Title: A new mechanism regulating microglial NLRP3 inflammasome: FMR1 mediates NLRP3 mRNA stability

doi: 10.1371/journal.pone.0341867

Figure Lengend Snippet: (A) Measurement of NLRP3, pro-caspase-1 and cleaved caspase-1 levels by western blot in BV2 cells transfected with FMR1 expression construct, FMR1 expression construct+NLRP3 cDNA plasmid, or vector control before LPS/ATP exposure. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Evaluation of caspase-1 activity in BV2 cells treated as indicated using the assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (C and D) Determination of IL-1β and IL-18 secretion levels by ELISA in the supernatant of BV2 cells treated as in A. Data are expressed as mean ± SD of 3 biologically independent experiments. (E) BV2 cells were transfected and treated as indicated, followed by LPS/ATP stimulation. The release of LDH into the culture supernatant was quantified as a marker of cell membrane integrity loss during pyroptosis. Data are expressed as mean ± SD of 3 biologically independent experiments. (F) FMR1 attenuates LPS/ATP-induced pyroptosis, as assessed by Calcein-AM/PI staining. Representative fluorescent micrographs (left) and quantification data (right). Nuclei were counterstained with DAPI (blue). Scale bar, 100 μm. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The levels of IL-1β and IL-18 in the supernatant of treated BV2 microglia were determined using Mouse IL-1β ELISA Kit (#EK201B) and Mouse IL-18 ELISA Kit (#EK218), respectively, as described by the vendor (Multi Sciences, Hangzhou, China).

Techniques: Western Blot, Transfection, Expressing, Construct, Plasmid Preparation, Control, Activity Assay, Enzyme-linked Immunosorbent Assay, Marker, Membrane, Staining

Journal: Frontiers in Physiology

Article Title: A miniaturized mouse extracorporeal circulation model to characterize early hematologic and metabolic alterations

doi: 10.3389/fphys.2026.1740282

Figure Lengend Snippet: ECC induced early systemic inflammatory responses and organ stress–associated biomarker changes. (A) Heatmap representation of plasma pro-inflammatory cytokine levels, including IL-1β, IL-18, IL-6, and TNF-α, measured in Control, Sham, and ECC groups at the end of the 60-min experimental period. Color intensity reflects relative concentration levels. Statistical comparisons among groups are indicated above the heatmap. (B) Heatmap comparison of plasma organ stress–associated biomarkers between Control and ECC groups at 60 min, including creatinine, cardiac troponin, AST/GOT, and LDH. Color intensity represents relative biomarker levels. P values for group comparisons are shown above each parameter. (C) Time-course analysis of myeloperoxidase (MPO) activity over a 30-min reaction period in plasma samples from Control, Sham, and ECC groups. MPO activity is expressed as optical density per minute (OD/min). ns, not significant.

Article Snippet: ELISA kits were obtained as follows: IL-1β (Cat. No. 88-7013a, Invitrogen, Thermo Fisher Scientific, United States), IL-6 (Cat. No. DY406, R&D Systems, United States), TNF-α (Cat. No. 88-7324, Invitrogen, Thermo Fisher Scientific, United States), and IL-18 (Cat. No. SEK50073 , Sino Biological Inc., China).

Techniques: Biomarker Discovery, Clinical Proteomics, Control, Concentration Assay, Comparison, Activity Assay

Journal: Scientific Reports

Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization

doi: 10.1038/s41598-026-38168-5

Figure Lengend Snippet: IL-18 expression in CP pancreatic tissues positively correlates with PF. (A) Immunofluorescence staining showed IL-18 expression and co-localization with acinar cells in human CP tissues compared to the normal pancreas ( n = 6). (B) IF for IL-18Rα in CP tissues ( n = 6). (C) Serum IL-18 concentrations in CP patients and controls measured by ELISA ( n = 8). (D) Histopathology (H&E) and fibrosis assessment by Masson’s trichrome ( n = 7). (E) IL-18 levels in pancreatic tissue homogenates from CP and normal samples ( n = 7–8). (F) Correlation analysis between tissue IL-18 expression and the fibrotic area in the same patient ( n = 7). ( G ) IL‑18 levels in PACs supernatants after CCK treatment. Data are mean ± SEM. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar = 50 μm. Ctrl control, CP chronic pancreatitis. PACs pancreatic acinar cells. CCK Cholecystokinins.

Article Snippet: To validate the in vivo role of IL-18 mediated through IL-4, we administered 500 ng of recombinant mouse IL-18 (rmIL-18; #HY- P73181 , MedChemExpress) intraperitoneally three times a week, starting two weeks after the initial caerulein injection.

Techniques: Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Histopathology, Control

Journal: Scientific Reports

Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization

doi: 10.1038/s41598-026-38168-5

Figure Lengend Snippet: IL-18 promotes IL-4 secretion by PSCs. (A , C) IF of human CP tissues showed IL-4 expression and co-localization with α-SMA ( n = 6). (B , D) Reduced pancreatic IL-4 expression in normal and chronic pancreatic tissues of both genotypes ( n = 3–5). (E) Schematic of primary murine PSC isolation and stimulation. (F) The purity of the extracted PSCs was evaluated by immunofluorescence detection of α-SMA. (G) PSCs were treated with rmIL-18, and qPCR was used to detect changes in the expression of IL-4, α-SMA, and TGF-β1 ( n = 5). (H) ELISA was used to measure changes in the IL-4 protein levels in the culture supernatant of PSCs treated with rmIL-18 ( n = 3). (I) Western blot results of PSCs after intervention Data are mean ± SEM. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar = 30 μm. NS normal saline, Ctrl control, CP chronic pancreatitis. PSC pancreatic stellate cells.

Article Snippet: To validate the in vivo role of IL-18 mediated through IL-4, we administered 500 ng of recombinant mouse IL-18 (rmIL-18; #HY- P73181 , MedChemExpress) intraperitoneally three times a week, starting two weeks after the initial caerulein injection.

Techniques: Expressing, Isolation, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Western Blot, Saline, Control

Journal: Scientific Reports

Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization

doi: 10.1038/s41598-026-38168-5

Figure Lengend Snippet: IL-18 drives M2 macrophage polarization via PSC-derived IL-4. (A) PSCs were cultured with or without rmIL-18, and then CM from different conditions were added to peritoneal macrophages seeded in plates. (B) The polarization of macrophages treated with CM, with or without the addition of IL-4 neutralizing antibody, was evaluated ( n = 3). (C , D) Western blot results of macrophages after intervention ( n = 3). (E , F) Quantitative PCR analysis of transcriptional levels of canonical M1 markers (iNOS, CD86) and M2 markers (CD206, YM-1) ( n = 3). Data are mean ± SEM. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar = 30 μm. Ctrl control, Mac macrophage, CM conditioned media.

Article Snippet: To validate the in vivo role of IL-18 mediated through IL-4, we administered 500 ng of recombinant mouse IL-18 (rmIL-18; #HY- P73181 , MedChemExpress) intraperitoneally three times a week, starting two weeks after the initial caerulein injection.

Techniques: Derivative Assay, Cell Culture, Western Blot, Real-time Polymerase Chain Reaction, Control

Journal: Scientific Reports

Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization

doi: 10.1038/s41598-026-38168-5

Figure Lengend Snippet: IL-18 exacerbates CP severity in vivo via the IL-4/M2 axis. (A) WT mice with caerulein-induced CP received rmIL-18 with or without IL-4 neutralizing antibody. H&E and Masson’s trichrome staining images with fibrosis quantification; pancreatic IL-4 assessed by IF ( n = 3–5). Scale bar = 30 μm (B , C) IF analysis of macrophage polarization markers in macrophages treated with rmIL-18, with or without IL-4 inhibition. ( n = 3–5). Data are mean ± SEM. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar = 50 μm. Ctrl control, CP chronic pancreatitis.

Article Snippet: To validate the in vivo role of IL-18 mediated through IL-4, we administered 500 ng of recombinant mouse IL-18 (rmIL-18; #HY- P73181 , MedChemExpress) intraperitoneally three times a week, starting two weeks after the initial caerulein injection.

Techniques: In Vivo, Staining, Inhibition, Control