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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) <t>Myeloperoxidase</t> <t>(MPO)</t> activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .
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Image Search Results


AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) Myeloperoxidase (MPO) activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .

Journal: Frontiers in Immunology

Article Title: Aqueous Artemisia argyi extract mitigates acute lung injury in association with coordinated alterations in gut microbiota, metabolic homeostasis, and pulmonary inflammatory gene expression

doi: 10.3389/fimmu.2026.1770675

Figure Lengend Snippet: AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) Myeloperoxidase (MPO) activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .

Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits for mouse IL-1β (Cat. #EK201B), IL-6 (Cat. #EK206), IL-10 (Cat. #EK210), TNF-α (Cat. #EK282), and myeloperoxidase (MPO) (Cat. #EK2133) were obtained from Multisciences (Lianke) Biotech Co., Ltd. (Hangzhou, China).

Techniques: Staining, Activity Assay