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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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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 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