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Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
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Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated <t>for</t> <t>IL-17A</t> in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).
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Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated <t>for</t> <t>IL-17A</t> in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).
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Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated <t>for</t> <t>IL-17A</t> in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).
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Oxidative stress and inflammatory markers in kidney tissue homogenates of different experimental groups showing levels of MDA ( A ), SOD ( B ), GSH ( C <t>),</t> <t>IL-17</t> ( D ), TNF-α ( E ), IL-6 ( F ) and CRP ( G ). Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test. Significant differences between groups are indicated by horizontal brackets, with asterisks denoting significance levels ( p < 0.05). ns = not significant
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Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection increases IL-17A content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway

Journal: Journal of Animal Science and Biotechnology

Article Title: Baicalin alleviates mastitis in dairy cows by targeting IL-17RA to inhibit IL-17 signaling pathway activation

doi: 10.1186/s40104-026-01401-2

Figure Lengend Snippet: Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection increases IL-17A content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway

Article Snippet: An in vitro mastitis model was established by treating cells with 5 μg/mL LPS (Sigma, USA) for 12 h. Baicalin (purity ≥ 95%) was purchased from Macklin (Shanghai, China), with a concentration of 20 μmol/L for 24 h. Furthermore, the TNFα inhibitor SPD304 and recombinant IL-17A (rIL-17A) were purchased from MedChemExpress (MCE, USA) and were used at concentrations of 5 μmol/L (for 2 h) and 100 ng/mL (for 12 h), respectively.

Techniques: In Vivo, Infection, Membrane, Activation Assay, Transduction

Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated for IL-17A in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).

Journal: Redox Biology

Article Title: Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals

doi: 10.1016/j.redox.2026.104105

Figure Lengend Snippet: Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated for IL-17A in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).

Article Snippet: IL-17A levels in BALF samples were measured using a commercially available Mouse IL-17A Sandwich ELISA Kit (Proteintech, Rosemont, IL; catalog# KE10020) according to the manufacturer's instructions.

Techniques:

Oxidative stress and inflammatory markers in kidney tissue homogenates of different experimental groups showing levels of MDA ( A ), SOD ( B ), GSH ( C ), IL-17 ( D ), TNF-α ( E ), IL-6 ( F ) and CRP ( G ). Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test. Significant differences between groups are indicated by horizontal brackets, with asterisks denoting significance levels ( p < 0.05). ns = not significant

Journal: Discover Nano

Article Title: Chitosan nanoparticle encapsulated pentoxifylline improves renal protection and reduces oxidative stress in amikacin induced nephrotoxicity

doi: 10.1186/s11671-026-04515-8

Figure Lengend Snippet: Oxidative stress and inflammatory markers in kidney tissue homogenates of different experimental groups showing levels of MDA ( A ), SOD ( B ), GSH ( C ), IL-17 ( D ), TNF-α ( E ), IL-6 ( F ) and CRP ( G ). Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test. Significant differences between groups are indicated by horizontal brackets, with asterisks denoting significance levels ( p < 0.05). ns = not significant

Article Snippet: 1,1-Diphenyl-2-picrylhydrazyl (DPPH) (Sigma-Aldrich, USA) Amikacin (AMK) (Sigma-Aldrich, USA) BioTek Synergy H1 Microplate Reader (BioTek, USA) Bruker D8 Advance X-ray Diffractometer (Bruker, USA) Bruker Tensor II FTIR Spectrometer (Bruker, Germany) Chitosan (medium molecular weight, ≥75% deacetylated) (Sigma-Aldrich, USA) Creatinine Assay Kit (ab65340) (Abcam, USA) Glutathione (GSH) Assay Kit (MBS267424) (MyBioSource, USA) Hitachi SU3500 SEM (Hitachi, Japan) IL-17 ELISA Kit (E-EL-M0047) (Elabscience, USA) JEOL JEM-1400Flash TEM (JEOL, Japan) Malondialdehyde (MDA) Assay Kit (MBS741034) (MyBioSource, USA) Malvern Zetasizer Nano ZS90 (Malvern Panalytical, UK) Pentoxifylline (PTX) (Sigma-Aldrich, USA) Shimadzu UV-1800 Spectrophotometer (Shimadzu, Japan) Sodium Tripolyphosphate (TPP) (Sigma-Aldrich, USA) Superoxide Dismutase (SOD) Assay Kit (MBS2707323) (MyBioSource, USA) Sysmex CA-560 Coagulation Analyzer (Sysmex, Japan) Urea Assay Kit (ab83362) (Abcam, USA) Uric Acid Assay Kit (ab65344) (Abcam, USA)

Techniques: