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recombinant mouse il 18  (MedChemExpress)


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    Structured Review

    MedChemExpress recombinant mouse il 18
    <t>IL-18</t> <t>expression</t> 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.
    Recombinant Mouse Il 18, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+mouse+il+18/IL-18%2C+Mouse/pmc12932839-51-16-23
    Average 93 stars, based on 1 article reviews
    recombinant mouse il 18 - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization"

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

    Journal: Scientific Reports

    doi: 10.1038/s41598-026-38168-5

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

    Techniques Used: In Vivo, Staining, Inhibition, Control

    Related Articles

    In Vivo:

    Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization
    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. .. To further neutralize IL-4, a concurrent intraperitoneal injection of 0.75 mg Ultra-LEAFTM Purified anti-mouse IL-4 antibody (#504138, BioLegend) was administered on the same schedule, beginning two weeks after the first caerulein injection.

    Recombinant:

    Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization
    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. .. To further neutralize IL-4, a concurrent intraperitoneal injection of 0.75 mg Ultra-LEAFTM Purified anti-mouse IL-4 antibody (#504138, BioLegend) was administered on the same schedule, beginning two weeks after the first caerulein injection.

    Article Title: Inhibition of NETs prevents doxorubicin-induced cardiotoxicity by attenuating IL-18-IFN-γ-Cx43 axis induced cardiac conduction abnormalities.
    Article Snippet: Doxorubicin-induced cardiotoxicity (DIC) is one of the most severe side effects of doxorubicin, yet the underlying mechanisms remain incompletely understood.. Our results showed that Neutrophil extracellular traps (NETs) accumulated in plasma and cardiac tissue after doxorubicin treatment.. The inhibition of NETs formation by Pad4 gene ablation significantly attenuated doxorubicin-induced arrhythmia, prolonged survival time and reduced the levels of Troponin T (cTnT) and creatine kinase MB (CK-MB) in mice.

    Injection:

    Article Title: IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization
    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. .. To further neutralize IL-4, a concurrent intraperitoneal injection of 0.75 mg Ultra-LEAFTM Purified anti-mouse IL-4 antibody (#504138, BioLegend) was administered on the same schedule, beginning two weeks after the first caerulein injection.



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    <t>IL-18</t> <t>expression</t> 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.
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    <t>IL-18</t> <t>expression</t> 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.
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    Image Search Results


    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.

    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

    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.

    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

    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.

    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

    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.

    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