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Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) <t>and</t> <t>ZO-1</t> (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.
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Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining <t>of</t> <t>ZO-1</t> (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.
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Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining <t>of</t> <t>ZO-1</t> (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.
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Effect of a high-salt diet (HSD) on atopic dermatitis (AD) severity, skin sodium, gut homeostasis, and type 1 interferon (IFN1) level. MC903 (45 μM, 20 μl/cm 2 ) or an equivalent SVT was topically applied to the exposed nape of 8- to 10-week-old mice (eight male mice per group) for 12 consecutive days. Mice received either normal-salt diet (NSD) or HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and the ileum <t>zonula</t> <t>occludens-1</t> <t>(ZO-1)</t> protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , skin sodium (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , the relative abundance of the main differential gut microbiota at the species level (G) , and the total serum IFN1 (H) levels are shown. Statistics: one-way ANOVA + Bonferonni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.
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Effect of a high-salt diet (HSD) on atopic dermatitis (AD) severity, skin sodium, gut homeostasis, and type 1 interferon (IFN1) level. MC903 (45 μM, 20 μl/cm 2 ) or an equivalent SVT was topically applied to the exposed nape of 8- to 10-week-old mice (eight male mice per group) for 12 consecutive days. Mice received either normal-salt diet (NSD) or HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and the ileum <t>zonula</t> <t>occludens-1</t> <t>(ZO-1)</t> protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , skin sodium (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , the relative abundance of the main differential gut microbiota at the species level (G) , and the total serum IFN1 (H) levels are shown. Statistics: one-way ANOVA + Bonferonni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.
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Effect of a high-salt diet (HSD) on atopic dermatitis (AD) severity, skin sodium, gut homeostasis, and type 1 interferon (IFN1) level. MC903 (45 μM, 20 μl/cm 2 ) or an equivalent SVT was topically applied to the exposed nape of 8- to 10-week-old mice (eight male mice per group) for 12 consecutive days. Mice received either normal-salt diet (NSD) or HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and the ileum <t>zonula</t> <t>occludens-1</t> <t>(ZO-1)</t> protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , skin sodium (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , the relative abundance of the main differential gut microbiota at the species level (G) , and the total serum IFN1 (H) levels are shown. Statistics: one-way ANOVA + Bonferonni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.
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EE restores intestinal barrier integrity and upregulates TJ protein expression. (A) Intestinal permeability was assessed using the FITC-dextran tracer assay. (B) Representative images of immunohistochemical staining <t>for</t> <t>ZO-1</t> and Occludin are displayed. Scale bar = 100 μm. (C) Quantification of immunofluorescence staining intensity for ZO-1 and Occludin. (D) Western blot analysis of TJ proteins (ZO-1 and Occludin) in colon tissues. (E) Densitometric analysis of protein levels shown in (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.
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EE restores intestinal barrier integrity and upregulates TJ protein expression. (A) Intestinal permeability was assessed using the FITC-dextran tracer assay. (B) Representative images of immunohistochemical staining <t>for</t> <t>ZO-1</t> and Occludin are displayed. Scale bar = 100 μm. (C) Quantification of immunofluorescence staining intensity for ZO-1 and Occludin. (D) Western blot analysis of TJ proteins (ZO-1 and Occludin) in colon tissues. (E) Densitometric analysis of protein levels shown in (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.
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Image Search Results


Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Article Snippet: The primary antibodies used included: ZO-1 ( GB111402 , Servicebio), Occludin (111401, Servicebio), PINK1 ( GB114934 , Servicebio), TOMM20 ( GB151481 , Servicebio), LC3B ( GB153801 , Servicebio), Beclin-1 ( GB115741 , Servicebio), CD206 ( GB113497 , Servicebio), PD-1 ( GB153744 , Servicebio), MPO ( GB150006 , Servicebio), and CD11b (GB15058, Servicebio).

Techniques: Ex Vivo, Fluorescence, Imaging, Labeling, In Vivo, Marker, Staining, Activity Assay, Immunofluorescence

Res-PD-L1@nmEVs Effectively Attenuates MRSA-Induced Pneumonia (A-B) Rats with MRSA-induced pneumonia received three bronchial nebulization treatments over one week with different formulations (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs). (A) Representative H&E-stained lung sections and (B) corresponding lung injury scores are shown (n = 5). (C) TUNEL staining of lung tissues to assess apoptosis. (D) Representative micro-CT images of anesthetized rats. (E-G) Flow cytometric analysis of immune cell proportions in lung single-cell suspensions: CD8 + T cells (E), neutrophils (F), and classical monocytes (G). (H-J) Plasma levels of inflammatory cytokines IL-6 (H), IL-1β (I), and TNF-α (J) (n = 5). (K) Immunofluorescence staining of tight junction proteins Occludin (green) and ZO-1 (red) in lung tissues (nuclei stained with DAPI). Scale bar: 50 μm. (L-N) Pulmonary function parameters: lung compliance (L), airway resistance (M), and oxygenation index (N) (n = 4). ∗ vs. Sham; # vs. MRSA; & vs. MRSA + PD-L1@nmEVs, p < 0.05.

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Effectively Attenuates MRSA-Induced Pneumonia (A-B) Rats with MRSA-induced pneumonia received three bronchial nebulization treatments over one week with different formulations (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs). (A) Representative H&E-stained lung sections and (B) corresponding lung injury scores are shown (n = 5). (C) TUNEL staining of lung tissues to assess apoptosis. (D) Representative micro-CT images of anesthetized rats. (E-G) Flow cytometric analysis of immune cell proportions in lung single-cell suspensions: CD8 + T cells (E), neutrophils (F), and classical monocytes (G). (H-J) Plasma levels of inflammatory cytokines IL-6 (H), IL-1β (I), and TNF-α (J) (n = 5). (K) Immunofluorescence staining of tight junction proteins Occludin (green) and ZO-1 (red) in lung tissues (nuclei stained with DAPI). Scale bar: 50 μm. (L-N) Pulmonary function parameters: lung compliance (L), airway resistance (M), and oxygenation index (N) (n = 4). ∗ vs. Sham; # vs. MRSA; & vs. MRSA + PD-L1@nmEVs, p < 0.05.

Article Snippet: The primary antibodies used included: ZO-1 ( GB111402 , Servicebio), Occludin (111401, Servicebio), PINK1 ( GB114934 , Servicebio), TOMM20 ( GB151481 , Servicebio), LC3B ( GB153801 , Servicebio), Beclin-1 ( GB115741 , Servicebio), CD206 ( GB113497 , Servicebio), PD-1 ( GB153744 , Servicebio), MPO ( GB150006 , Servicebio), and CD11b (GB15058, Servicebio).

Techniques: Staining, TUNEL Assay, Micro-CT, Single Cell, Clinical Proteomics, Immunofluorescence

Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining of ZO-1 (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining of ZO-1 (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.

Article Snippet: Immunofluorescence staining of CK14 (Abcam, ab181595), AC-Tub (Proteintech, 66200-1-Ig), ZO-1 (Proteintech, 21773-1-AP), and Immunohistochemical (IHC) staining for CD31 (Servicebio, S1002) were conducted to reveal the conditions of mucosal regeneration, according to previous literature [ ].

Techniques: Staining, Marker

Effect of a high-salt diet (HSD) on atopic dermatitis (AD) severity, skin sodium, gut homeostasis, and type 1 interferon (IFN1) level. MC903 (45 μM, 20 μl/cm 2 ) or an equivalent SVT was topically applied to the exposed nape of 8- to 10-week-old mice (eight male mice per group) for 12 consecutive days. Mice received either normal-salt diet (NSD) or HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and the ileum zonula occludens-1 (ZO-1) protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , skin sodium (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , the relative abundance of the main differential gut microbiota at the species level (G) , and the total serum IFN1 (H) levels are shown. Statistics: one-way ANOVA + Bonferonni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gut Lactobacillus -maintained systemic type 1 interferon

doi: 10.3389/fcimb.2026.1794494

Figure Lengend Snippet: Effect of a high-salt diet (HSD) on atopic dermatitis (AD) severity, skin sodium, gut homeostasis, and type 1 interferon (IFN1) level. MC903 (45 μM, 20 μl/cm 2 ) or an equivalent SVT was topically applied to the exposed nape of 8- to 10-week-old mice (eight male mice per group) for 12 consecutive days. Mice received either normal-salt diet (NSD) or HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and the ileum zonula occludens-1 (ZO-1) protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , skin sodium (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , the relative abundance of the main differential gut microbiota at the species level (G) , and the total serum IFN1 (H) levels are shown. Statistics: one-way ANOVA + Bonferonni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The antibodies were anti-NEDD4L (no. A8085; ABclonal, Woburn, MA, USA), anti-phosphorylated NEDD4L (Ser448, no. AP0843; ABclonal), anti-GAPDH (no. A19056; Abclonal), anti-vinculin (no. AG3539; Beyotime, Shanghai, China), anti-SGK1 (no. 12103; CST, Danvers, MA, USA), phosphorylated SGK1 (Ser78, no. 5599; CST), anti-αENaC (no. ab272878; Abcam), anti-βENaC (no. A1765; Abclonal), anti-γENaC (no. A15097; Abclonal), and anti-zonula occludens-1 (ZO-1) (no. GB151981 ; Servicebio, Wuhan, China).

Techniques: Staining, Expressing

Effect of Lactobacillus supplementation on atopic dermatitis (AD) and its correlation with gut homeostasis and the type 1 interferon (IFN1) level in mice receiving a high-salt diet (HSD). MC903 (45 μM, 20 μl/cm 2 ) was topically applied to the exposed nape of wild-type ( wt ) or Ifnar1 knockout ( Ifnar1 KO ) mice (8–10 weeks old, eight male mice per group) for 12 consecutive days. Mice synchronously received HSD and SVT or Lactobacillus ( Lactob ) supplementation for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and ileum zonula occludens-1 (ZO-1) protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , total serum IFN1 level (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , and the relative abundance of the main differential gut microbiota at species level (G) are shown. Statistics: One-way ANOVA + Bonferroni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gut Lactobacillus -maintained systemic type 1 interferon

doi: 10.3389/fcimb.2026.1794494

Figure Lengend Snippet: Effect of Lactobacillus supplementation on atopic dermatitis (AD) and its correlation with gut homeostasis and the type 1 interferon (IFN1) level in mice receiving a high-salt diet (HSD). MC903 (45 μM, 20 μl/cm 2 ) was topically applied to the exposed nape of wild-type ( wt ) or Ifnar1 knockout ( Ifnar1 KO ) mice (8–10 weeks old, eight male mice per group) for 12 consecutive days. Mice synchronously received HSD and SVT or Lactobacillus ( Lactob ) supplementation for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Skin lesions, hematoxylin–eosin (HE) staining of the lesions, and ileum zonula occludens-1 (ZO-1) protein expression (A) (bar represents 100 μm), serum IgE (B) , serum IL-4 and IL-13 (C) , total serum IFN1 level (D) , related proteins in the ileum (E) , β-diversity based on principal coordinate analysis (F) , and the relative abundance of the main differential gut microbiota at species level (G) are shown. Statistics: One-way ANOVA + Bonferroni’s tests. n.s., p > 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The antibodies were anti-NEDD4L (no. A8085; ABclonal, Woburn, MA, USA), anti-phosphorylated NEDD4L (Ser448, no. AP0843; ABclonal), anti-GAPDH (no. A19056; Abclonal), anti-vinculin (no. AG3539; Beyotime, Shanghai, China), anti-SGK1 (no. 12103; CST, Danvers, MA, USA), phosphorylated SGK1 (Ser78, no. 5599; CST), anti-αENaC (no. ab272878; Abcam), anti-βENaC (no. A1765; Abclonal), anti-γENaC (no. A15097; Abclonal), and anti-zonula occludens-1 (ZO-1) (no. GB151981 ; Servicebio, Wuhan, China).

Techniques: Knock-Out, Staining, Expressing

Role of intestinal epithelial cell (IEC)-specific SGK1 signaling in atopic dermatitis (AD) and its correlation with the gut homeostasis and type 1 interferon (IFN1) level in mice receiving a high-salt diet (HSD) or a normal-salt diet (NSD). MC903 (45 μM, 20 μl/cm 2 ) was topically applied to the exposed nape of mice with sgk1 ( f/f ) or sgk1 ( f/f );Vil1 Cre (8–10 weeks old, eight male mice per group) for 12 consecutive days. Mice received HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Epidermal thickness (A) , serum IgE (B) , serum IL-4 and IL-13 (C) , and total serum IFN1 level (D) , skin sodium (E) , ileum zonula occludens-1 (ZO-1) protein expression (F) , related proteins in the ileum (G) , and the relative abundance of main the differential gut microbiota at the species level (H) are shown. Statistics: One-way ANOVA + Bonferroni’s tests. n.s., p > 0.05; *** p < 0.001.

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gut Lactobacillus -maintained systemic type 1 interferon

doi: 10.3389/fcimb.2026.1794494

Figure Lengend Snippet: Role of intestinal epithelial cell (IEC)-specific SGK1 signaling in atopic dermatitis (AD) and its correlation with the gut homeostasis and type 1 interferon (IFN1) level in mice receiving a high-salt diet (HSD) or a normal-salt diet (NSD). MC903 (45 μM, 20 μl/cm 2 ) was topically applied to the exposed nape of mice with sgk1 ( f/f ) or sgk1 ( f/f );Vil1 Cre (8–10 weeks old, eight male mice per group) for 12 consecutive days. Mice received HSD for 2 weeks prior to and during MC903 application. The mice were then anesthetized and related samples were obtained. Epidermal thickness (A) , serum IgE (B) , serum IL-4 and IL-13 (C) , and total serum IFN1 level (D) , skin sodium (E) , ileum zonula occludens-1 (ZO-1) protein expression (F) , related proteins in the ileum (G) , and the relative abundance of main the differential gut microbiota at the species level (H) are shown. Statistics: One-way ANOVA + Bonferroni’s tests. n.s., p > 0.05; *** p < 0.001.

Article Snippet: The antibodies were anti-NEDD4L (no. A8085; ABclonal, Woburn, MA, USA), anti-phosphorylated NEDD4L (Ser448, no. AP0843; ABclonal), anti-GAPDH (no. A19056; Abclonal), anti-vinculin (no. AG3539; Beyotime, Shanghai, China), anti-SGK1 (no. 12103; CST, Danvers, MA, USA), phosphorylated SGK1 (Ser78, no. 5599; CST), anti-αENaC (no. ab272878; Abcam), anti-βENaC (no. A1765; Abclonal), anti-γENaC (no. A15097; Abclonal), and anti-zonula occludens-1 (ZO-1) (no. GB151981 ; Servicebio, Wuhan, China).

Techniques: Expressing

EE restores intestinal barrier integrity and upregulates TJ protein expression. (A) Intestinal permeability was assessed using the FITC-dextran tracer assay. (B) Representative images of immunohistochemical staining for ZO-1 and Occludin are displayed. Scale bar = 100 μm. (C) Quantification of immunofluorescence staining intensity for ZO-1 and Occludin. (D) Western blot analysis of TJ proteins (ZO-1 and Occludin) in colon tissues. (E) Densitometric analysis of protein levels shown in (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Journal: Frontiers in Medicine

Article Title: Earthworm extract ameliorates colitis via modulation of the PI3K/AKT pathway: attenuation of inflammation and restoration of intestinal barrier integrity

doi: 10.3389/fmed.2026.1787022

Figure Lengend Snippet: EE restores intestinal barrier integrity and upregulates TJ protein expression. (A) Intestinal permeability was assessed using the FITC-dextran tracer assay. (B) Representative images of immunohistochemical staining for ZO-1 and Occludin are displayed. Scale bar = 100 μm. (C) Quantification of immunofluorescence staining intensity for ZO-1 and Occludin. (D) Western blot analysis of TJ proteins (ZO-1 and Occludin) in colon tissues. (E) Densitometric analysis of protein levels shown in (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies against ZO-1 (Servicebio, 1:200) and Occludin (Proteintech, 1:400).

Techniques: Expressing, Permeability, Immunohistochemical staining, Staining, Immunofluorescence, Western Blot

EE protects intestinal epithelial cells against LPS-induced barrier disruption via anti-inflammatory and junction-enhancing. (A) Cell viability of Caco-2 cells treated with EE (25, 50, 100 μg/mL) for 24, 48, and 72 h, as assessed by the CCK-8 assay. (B) Relative mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) in Caco-2 cells following LPS stimulation with or without EE pretreatment. (C) Transepithelial electrical resistance (TEER) of Caco-2 monolayers after LPS challenge in the presence or absence of EE. (D,E) Immunofluorescence staining showing the distribution of ZO-1 (green) and Occludin (red) in Caco-2 monolayers, with nuclei counterstained by DAPI (blue), and corresponding quantitative analysis of fluorescence intensity. (F,G) Western blot analysis of ZO-1 and Occludin protein expression (F) and densitometric quantification of the immunoblots (G) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Medicine

Article Title: Earthworm extract ameliorates colitis via modulation of the PI3K/AKT pathway: attenuation of inflammation and restoration of intestinal barrier integrity

doi: 10.3389/fmed.2026.1787022

Figure Lengend Snippet: EE protects intestinal epithelial cells against LPS-induced barrier disruption via anti-inflammatory and junction-enhancing. (A) Cell viability of Caco-2 cells treated with EE (25, 50, 100 μg/mL) for 24, 48, and 72 h, as assessed by the CCK-8 assay. (B) Relative mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) in Caco-2 cells following LPS stimulation with or without EE pretreatment. (C) Transepithelial electrical resistance (TEER) of Caco-2 monolayers after LPS challenge in the presence or absence of EE. (D,E) Immunofluorescence staining showing the distribution of ZO-1 (green) and Occludin (red) in Caco-2 monolayers, with nuclei counterstained by DAPI (blue), and corresponding quantitative analysis of fluorescence intensity. (F,G) Western blot analysis of ZO-1 and Occludin protein expression (F) and densitometric quantification of the immunoblots (G) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies against ZO-1 (Servicebio, 1:200) and Occludin (Proteintech, 1:400).

Techniques: Disruption, CCK-8 Assay, Expressing, Immunofluorescence, Staining, Fluorescence, Western Blot

Pharmacological activation of PI3K abolishes the therapeutic effects of EE in DSS-induced colitis. (A) Body weight changes across experimental groups. (B) DAI score. (C,D) Representative colon images (C) and quantified colon length (D) at the endpoint. (E,F) Representative H&E-stained colon sections ( E ; scale bar = 200 μm) and corresponding histopathological scores (F) . (G) Intestinal permeability assessed by serum FITC-dextran flux. (H) Serum levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) measured by ELISA. (I,J) Western blot analysis of p-AKT, p-PI3K, p-p65, Occludin, and ZO-1 protein expression (I) and densitometric quantification of the immunoblots (J) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Journal: Frontiers in Medicine

Article Title: Earthworm extract ameliorates colitis via modulation of the PI3K/AKT pathway: attenuation of inflammation and restoration of intestinal barrier integrity

doi: 10.3389/fmed.2026.1787022

Figure Lengend Snippet: Pharmacological activation of PI3K abolishes the therapeutic effects of EE in DSS-induced colitis. (A) Body weight changes across experimental groups. (B) DAI score. (C,D) Representative colon images (C) and quantified colon length (D) at the endpoint. (E,F) Representative H&E-stained colon sections ( E ; scale bar = 200 μm) and corresponding histopathological scores (F) . (G) Intestinal permeability assessed by serum FITC-dextran flux. (H) Serum levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) measured by ELISA. (I,J) Western blot analysis of p-AKT, p-PI3K, p-p65, Occludin, and ZO-1 protein expression (I) and densitometric quantification of the immunoblots (J) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies against ZO-1 (Servicebio, 1:200) and Occludin (Proteintech, 1:400).

Techniques: Activation Assay, Staining, Permeability, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

Pharmacological activation of PI3K abolishes the protective effects of EE in TNF-α/IFN-γ-stimulated Caco-2 cells. (A) TEER of Caco-2 monolayers after TNF-α/IFN-γ challenge with or without EE (50 μg/mL) in the absence or presence of 740Y-P (10 μm) for 24 h. (B) Relative mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6). (C,D) Western blot analysis of p-AKT, p-PI3K, p-p65, Occludin, and ZO-1 protein expression (C) and densitometric quantification of the immunoblots (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Journal: Frontiers in Medicine

Article Title: Earthworm extract ameliorates colitis via modulation of the PI3K/AKT pathway: attenuation of inflammation and restoration of intestinal barrier integrity

doi: 10.3389/fmed.2026.1787022

Figure Lengend Snippet: Pharmacological activation of PI3K abolishes the protective effects of EE in TNF-α/IFN-γ-stimulated Caco-2 cells. (A) TEER of Caco-2 monolayers after TNF-α/IFN-γ challenge with or without EE (50 μg/mL) in the absence or presence of 740Y-P (10 μm) for 24 h. (B) Relative mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6). (C,D) Western blot analysis of p-AKT, p-PI3K, p-p65, Occludin, and ZO-1 protein expression (C) and densitometric quantification of the immunoblots (D) . Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies against ZO-1 (Servicebio, 1:200) and Occludin (Proteintech, 1:400).

Techniques: Activation Assay, Expressing, Western Blot