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Servicebio Inc antibody anti rabbit cd68
Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of <t>CD68</t> + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
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1) Product Images from "Gut microbiota-derived xanthohumol protects against heatstroke by inhibiting macrophage pyroptosis in mice"

Article Title: Gut microbiota-derived xanthohumol protects against heatstroke by inhibiting macrophage pyroptosis in mice

Journal: Journal of Advanced Research

doi: 10.1016/j.jare.2025.07.031

Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
Figure Legend Snippet: Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.

Techniques Used: Bacteria, Clinical Proteomics, Concentration Assay, Staining, TUNEL Assay, Two Tailed Test

Gut microbiota-derived XN protects against heatstroke in a murine model. (A) Schematic process of the XN administration: heatstroke-treated mice were pretreated with XN orally once a day for 3 days. Tissue samples were harvested 12 h later. (B) Plasma ALT, AST, and Cr levels, and MPO activity in the lung. Experimental design as in (3A). n = 7. (C) H&E staining and histopathological scores of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (D) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (E) The serum levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (3A). n = 6. (F) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (3A). Scale bars, 100 μm. n = 6. Data are represented as the mean ± SEM. * p < 0.05 were determined by one-way ANOVA (Tukey's test) in B–F.
Figure Legend Snippet: Gut microbiota-derived XN protects against heatstroke in a murine model. (A) Schematic process of the XN administration: heatstroke-treated mice were pretreated with XN orally once a day for 3 days. Tissue samples were harvested 12 h later. (B) Plasma ALT, AST, and Cr levels, and MPO activity in the lung. Experimental design as in (3A). n = 7. (C) H&E staining and histopathological scores of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (D) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (E) The serum levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (3A). n = 6. (F) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (3A). Scale bars, 100 μm. n = 6. Data are represented as the mean ± SEM. * p < 0.05 were determined by one-way ANOVA (Tukey's test) in B–F.

Techniques Used: Derivative Assay, Clinical Proteomics, Activity Assay, Staining, TUNEL Assay



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Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of <t>CD68</t> + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
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Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of <t>CD68</t> + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
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Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of <t>CD68</t> + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
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Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of <t>CD68</t> + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.
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a The relative mRNA levels of essential Trp metabolic enzymes (to β-actin ) in liver were determined using RT–qPCR ( n = 6). b The Trp metabolites in plasma ( n = 6). c , d The relative mRNA levels of Ahr , Cyp1a1 and Cyp1b1 (to β-actin ) in liver ( c ) and colon ( d ) were determined using RT–qPCR ( n = 6). e Immunofluorescence of aortic root cross-sections demonstrating staining for Ahr in plaques. Scale bar, 200 μm. f Psrc1 protein expression in Raw264.7, MOVAS and MAEC determined by western blotting. g Immunofluorescence of aortic root cross-sections demonstrating staining for Psrc1 in <t>CD68</t> + macrophages and α-SMA + smooth muscle cells. Scale bar, 150 μm. h Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice. Scale bar, 50 μm (top) and 10 μm (bottom). Data are presented as mean ± s.d. Statistical analysis was performed by two-tailed unpaired t- tests ( Ido1 , Ido2 , Kynu , Kmo , Mao , Kat1 , Kat2 and Kat3 in a and b and Ahr in c and d ) and Mann–Whitney U test ( Tdo and Tph1 in a and Cyp1a1 and Cyp1b1 in c ).
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a The relative mRNA levels of essential Trp metabolic enzymes (to β-actin ) in liver were determined using RT–qPCR ( n = 6). b The Trp metabolites in plasma ( n = 6). c , d The relative mRNA levels of Ahr , Cyp1a1 and Cyp1b1 (to β-actin ) in liver ( c ) and colon ( d ) were determined using RT–qPCR ( n = 6). e Immunofluorescence of aortic root cross-sections demonstrating staining for Ahr in plaques. Scale bar, 200 μm. f Psrc1 protein expression in Raw264.7, MOVAS and MAEC determined by western blotting. g Immunofluorescence of aortic root cross-sections demonstrating staining for Psrc1 in <t>CD68</t> + macrophages and α-SMA + smooth muscle cells. Scale bar, 150 μm. h Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice. Scale bar, 50 μm (top) and 10 μm (bottom). Data are presented as mean ± s.d. Statistical analysis was performed by two-tailed unpaired t- tests ( Ido1 , Ido2 , Kynu , Kmo , Mao , Kat1 , Kat2 and Kat3 in a and b and Ahr in c and d ) and Mann–Whitney U test ( Tdo and Tph1 in a and Cyp1a1 and Cyp1b1 in c ).
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Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.

Journal: Journal of Advanced Research

Article Title: Gut microbiota-derived xanthohumol protects against heatstroke by inhibiting macrophage pyroptosis in mice

doi: 10.1016/j.jare.2025.07.031

Figure Lengend Snippet: Dysbiosis of the gut microbiota contributes to heatstroke-induced organ injury in mice. (A) PCoA plot based on the weighted UniFrac distance matrices in mice treated with or without heatstroke. n = 8. (B–C) Relative abundance of bacteria at the phylum level (B) and the genus level (C) in the cecal contents of mice. n = 8. (D) LEfSe analysis between the two groups. n = 8. (E) Schematic process of FMT experiment. Tissue samples were harvested 12 h later. (F) Plasma concentration of ALT, AST, and Cr, and total protein contents in BALF. Experimental design as in (1E). n = 5. (G) H&E staining of the liver, kidney, and lung. The box plots showed the quantitative analysis histopathological score in each group. Scale bars, 100 μm. n = 6. (H) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (1E). Scale bars, 100 μm. n = 6. (I) Plasma levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (1E). n = 5–6. (J) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (1E). Scale bars, 100 μm. n = 5–6. Data are represented as the mean ± SEM. * p < 0.05 were determined by adonis analysis and anosim analysis in A, two-tailed Student's t -test in F–J.

Article Snippet: Then, each lung slide was treated with primary antibody anti-rabbit CD68 (Servicebio, China) at 4°C overnight.

Techniques: Bacteria, Clinical Proteomics, Concentration Assay, Staining, TUNEL Assay, Two Tailed Test

Gut microbiota-derived XN protects against heatstroke in a murine model. (A) Schematic process of the XN administration: heatstroke-treated mice were pretreated with XN orally once a day for 3 days. Tissue samples were harvested 12 h later. (B) Plasma ALT, AST, and Cr levels, and MPO activity in the lung. Experimental design as in (3A). n = 7. (C) H&E staining and histopathological scores of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (D) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (E) The serum levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (3A). n = 6. (F) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (3A). Scale bars, 100 μm. n = 6. Data are represented as the mean ± SEM. * p < 0.05 were determined by one-way ANOVA (Tukey's test) in B–F.

Journal: Journal of Advanced Research

Article Title: Gut microbiota-derived xanthohumol protects against heatstroke by inhibiting macrophage pyroptosis in mice

doi: 10.1016/j.jare.2025.07.031

Figure Lengend Snippet: Gut microbiota-derived XN protects against heatstroke in a murine model. (A) Schematic process of the XN administration: heatstroke-treated mice were pretreated with XN orally once a day for 3 days. Tissue samples were harvested 12 h later. (B) Plasma ALT, AST, and Cr levels, and MPO activity in the lung. Experimental design as in (3A). n = 7. (C) H&E staining and histopathological scores of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (D) TUNEL staining and quantification of dead cells of the liver, kidney, and lung. Experimental design as in (3A). Scale bars, 100 μm. n = 7. (E) The serum levels of TNF-α, IL-1β, and IL-6 in each group. Experimental design as in (3A). n = 6. (F) Immunohistological staining of and quantification of CD68 + cells in the lung tissue. Experimental design as in (3A). Scale bars, 100 μm. n = 6. Data are represented as the mean ± SEM. * p < 0.05 were determined by one-way ANOVA (Tukey's test) in B–F.

Article Snippet: Then, each lung slide was treated with primary antibody anti-rabbit CD68 (Servicebio, China) at 4°C overnight.

Techniques: Derivative Assay, Clinical Proteomics, Activity Assay, Staining, TUNEL Assay

a The relative mRNA levels of essential Trp metabolic enzymes (to β-actin ) in liver were determined using RT–qPCR ( n = 6). b The Trp metabolites in plasma ( n = 6). c , d The relative mRNA levels of Ahr , Cyp1a1 and Cyp1b1 (to β-actin ) in liver ( c ) and colon ( d ) were determined using RT–qPCR ( n = 6). e Immunofluorescence of aortic root cross-sections demonstrating staining for Ahr in plaques. Scale bar, 200 μm. f Psrc1 protein expression in Raw264.7, MOVAS and MAEC determined by western blotting. g Immunofluorescence of aortic root cross-sections demonstrating staining for Psrc1 in CD68 + macrophages and α-SMA + smooth muscle cells. Scale bar, 150 μm. h Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice. Scale bar, 50 μm (top) and 10 μm (bottom). Data are presented as mean ± s.d. Statistical analysis was performed by two-tailed unpaired t- tests ( Ido1 , Ido2 , Kynu , Kmo , Mao , Kat1 , Kat2 and Kat3 in a and b and Ahr in c and d ) and Mann–Whitney U test ( Tdo and Tph1 in a and Cyp1a1 and Cyp1b1 in c ).

Journal: Experimental & Molecular Medicine

Article Title: Proline/serine-rich coiled-coil 1 alleviates atherosclerosis via remodeling tryptophan metabolism mediated by Akkermansia muciniphila

doi: 10.1038/s12276-026-01668-5

Figure Lengend Snippet: a The relative mRNA levels of essential Trp metabolic enzymes (to β-actin ) in liver were determined using RT–qPCR ( n = 6). b The Trp metabolites in plasma ( n = 6). c , d The relative mRNA levels of Ahr , Cyp1a1 and Cyp1b1 (to β-actin ) in liver ( c ) and colon ( d ) were determined using RT–qPCR ( n = 6). e Immunofluorescence of aortic root cross-sections demonstrating staining for Ahr in plaques. Scale bar, 200 μm. f Psrc1 protein expression in Raw264.7, MOVAS and MAEC determined by western blotting. g Immunofluorescence of aortic root cross-sections demonstrating staining for Psrc1 in CD68 + macrophages and α-SMA + smooth muscle cells. Scale bar, 150 μm. h Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice. Scale bar, 50 μm (top) and 10 μm (bottom). Data are presented as mean ± s.d. Statistical analysis was performed by two-tailed unpaired t- tests ( Ido1 , Ido2 , Kynu , Kmo , Mao , Kat1 , Kat2 and Kat3 in a and b and Ahr in c and d ) and Mann–Whitney U test ( Tdo and Tph1 in a and Cyp1a1 and Cyp1b1 in c ).

Article Snippet: The macrophage and smooth muscle cells in plaques were detected via immunofluorescence staining with antibodies against CD68 (97778S, CST) and α-SMA (19245S, CST), respectively.

Techniques: Quantitative RT-PCR, Clinical Proteomics, Immunofluorescence, Staining, Expressing, Western Blot, Isolation, Two Tailed Test, MANN-WHITNEY

a The experimental design showing groups and durations. Eight-week-old male Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice fed a HFD for 12 weeks. Mice were orally gavaged with antibiotic cocktail for 2 weeks and subsequently with live A. muciniphila strain or heat-killed A. muciniphila or PBS for 4 weeks during the last 6 weeks. b Representative images of ORO staining and quantitative analysis of the atherosclerotic plaques area en face aorta ( n = 10). c–e Representative photomicrograph of ORO ( c ), HE ( d ) and Masson’s trichrome ( e ) staining and quantification of lipid accumulation, atherosclerotic plaques area, necrotic core and collagen content in aortic roots ( n = 10). Scale bar, 200 μm. f Immunofluorescence of aortic root cross-sections demonstrating staining α-SMA for smooth muscle cells and DAPI for nuclei ( n = 6). Scale bar, 200 μm. g The plasma IAA levels were determined by ELISA ( n = 10). h The relative mRNA levels of Cyp1a1 (to β-actin ) in MPM isolated from mice were determined using RT–qPCR ( n = 6). i Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from mice ( n = 6). Scale bar, 50 μm. j Immunofluorescence of aortic root cross-sections demonstrating staining CD68 and Ahr to detect macrophage infiltration and Ahr in macrophages ( n = 6). Scale bar, 200 μm. Data are presented as mean ± s.d. P values were determined by two-way ANOVA followed by Tukey’s post hoc test ( b , c, d (top), e , f and j ) or Tamhane’s T2 post hoc test ( d (bottom), g and h ).

Journal: Experimental & Molecular Medicine

Article Title: Proline/serine-rich coiled-coil 1 alleviates atherosclerosis via remodeling tryptophan metabolism mediated by Akkermansia muciniphila

doi: 10.1038/s12276-026-01668-5

Figure Lengend Snippet: a The experimental design showing groups and durations. Eight-week-old male Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice fed a HFD for 12 weeks. Mice were orally gavaged with antibiotic cocktail for 2 weeks and subsequently with live A. muciniphila strain or heat-killed A. muciniphila or PBS for 4 weeks during the last 6 weeks. b Representative images of ORO staining and quantitative analysis of the atherosclerotic plaques area en face aorta ( n = 10). c–e Representative photomicrograph of ORO ( c ), HE ( d ) and Masson’s trichrome ( e ) staining and quantification of lipid accumulation, atherosclerotic plaques area, necrotic core and collagen content in aortic roots ( n = 10). Scale bar, 200 μm. f Immunofluorescence of aortic root cross-sections demonstrating staining α-SMA for smooth muscle cells and DAPI for nuclei ( n = 6). Scale bar, 200 μm. g The plasma IAA levels were determined by ELISA ( n = 10). h The relative mRNA levels of Cyp1a1 (to β-actin ) in MPM isolated from mice were determined using RT–qPCR ( n = 6). i Representative images of immunofluorescence staining of Ahr protein and DAPI for nuclei in MPM isolated from mice ( n = 6). Scale bar, 50 μm. j Immunofluorescence of aortic root cross-sections demonstrating staining CD68 and Ahr to detect macrophage infiltration and Ahr in macrophages ( n = 6). Scale bar, 200 μm. Data are presented as mean ± s.d. P values were determined by two-way ANOVA followed by Tukey’s post hoc test ( b , c, d (top), e , f and j ) or Tamhane’s T2 post hoc test ( d (bottom), g and h ).

Article Snippet: The macrophage and smooth muscle cells in plaques were detected via immunofluorescence staining with antibodies against CD68 (97778S, CST) and α-SMA (19245S, CST), respectively.

Techniques: Staining, Immunofluorescence, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Isolation, Quantitative RT-PCR

a The experimental design showing groups and durations. Eight-week-old male Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice fed a HFD for 12 weeks. Psrc1 +/+ Apoe −/− mice were orally administrated with vehicle or IAA (50 mg/kg/day) or atorvastatin (15 mg/kg/day), while Psrc1 −/− Apoe − / − were orally administrated with vehicle or IAA individually or IAA with CH-223191 (10 mg/kg/day) during the last 4 weeks. b Representative images of ORO staining and quantitative analysis of the atherosclerotic plaques area en face aorta ( n = 6 in the atorvastatin group, n = 10 in other groups). c–e Representative photomicrograph of ORO ( c ), HE ( d ) and Masson’s trichrome ( e ) staining and quantification of lipid accumulation, atherosclerotic plaques area, necrotic core and collagen content in aortic roots ( n = 6 in the atorvastatin group, n = 10 in other groups). Scale bar, 200 μm. f Immunofluorescence of aortic root cross-sections demonstrating staining α-SMA for smooth muscle cells and DAPI for nuclei ( n = 6). Scale bar, 200 μm. g Immunofluorescence of aortic root cross-sections demonstrating staining for CD68 and TUNEL to detect macrophage infiltration and apoptotic macrophages ( n = 6). Scale bar, 200 μm. Data are presented as mean ± s.d. P values were determined by one-way ANOVA followed by Tukey’s post hoc test.

Journal: Experimental & Molecular Medicine

Article Title: Proline/serine-rich coiled-coil 1 alleviates atherosclerosis via remodeling tryptophan metabolism mediated by Akkermansia muciniphila

doi: 10.1038/s12276-026-01668-5

Figure Lengend Snippet: a The experimental design showing groups and durations. Eight-week-old male Psrc1 +/+ Apoe −/− and Psrc1 −/− Apoe −/− mice fed a HFD for 12 weeks. Psrc1 +/+ Apoe −/− mice were orally administrated with vehicle or IAA (50 mg/kg/day) or atorvastatin (15 mg/kg/day), while Psrc1 −/− Apoe − / − were orally administrated with vehicle or IAA individually or IAA with CH-223191 (10 mg/kg/day) during the last 4 weeks. b Representative images of ORO staining and quantitative analysis of the atherosclerotic plaques area en face aorta ( n = 6 in the atorvastatin group, n = 10 in other groups). c–e Representative photomicrograph of ORO ( c ), HE ( d ) and Masson’s trichrome ( e ) staining and quantification of lipid accumulation, atherosclerotic plaques area, necrotic core and collagen content in aortic roots ( n = 6 in the atorvastatin group, n = 10 in other groups). Scale bar, 200 μm. f Immunofluorescence of aortic root cross-sections demonstrating staining α-SMA for smooth muscle cells and DAPI for nuclei ( n = 6). Scale bar, 200 μm. g Immunofluorescence of aortic root cross-sections demonstrating staining for CD68 and TUNEL to detect macrophage infiltration and apoptotic macrophages ( n = 6). Scale bar, 200 μm. Data are presented as mean ± s.d. P values were determined by one-way ANOVA followed by Tukey’s post hoc test.

Article Snippet: The macrophage and smooth muscle cells in plaques were detected via immunofluorescence staining with antibodies against CD68 (97778S, CST) and α-SMA (19245S, CST), respectively.

Techniques: Staining, Immunofluorescence, TUNEL Assay