Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: AKK alleviates ABX/LPS-induced pathological remodeling and inflammation in murine intestine via inhibition of the p38α MAPK pathway. (A) Schematic of the experimental design, illustrating the timeline of ABX/LPS challenge and the interventions with AKK or the p38α MAPK inhibitor (SB203580). (B) Body weight changes of mice in different treatment groups. (C) Disease activity index. The data points represent the daily measurements. To make the graph clear, the data at key time points are shown in the figure. (D) Representative images showing: (i) The gross appearance of the colon and cecum; (ii) H&E-stained sections of the ileum; and (iii) H&E-stained sections of the colon. (E) Quantitative analysis of colon length. (F) Histopathological colitis scores. (G–I) Morphometric analysis of the ileum, including villus height, crypt depth, and the villus height-to-crypt depth ratio (VCR). n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus NC group; * p < 0.05, ** p > p < 0.01, *** p < 0.001, **** p < 0.0001 versus NS + ABX/LPS group, + p < 0.05, ++ p < 0.01, +++ p < 0.01, +++ p < 0.001, +++p < 0.0001 versus the AKK-treated group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Inhibition, Activity Assay, Staining

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: AKK directly inhibits phosphorylation and activation of p38α MAPK in human colonic epithelial cells. In the LPS-induced injury model of Ncm460 cells: (A) Identification of the optimal concentration and treatment time for AKK via CCK-8 assay. (B) AKK reverses the LPS-induced suppression of cell viability. Data are normalized to the control group (set as 1.0). (C) Representative western blot images of p38α MAPK and phosphorylated p38α MAPK (p-p38α MAPK). Blots for p38α MAPK and p-p38α MAPK were obtained from the same membrane. (D) Quantitative analysis of total p-p38α MAPK protein expression levels. n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus p38KD group. * p < 0.05, ** p > p < 0.01, *** p < 0.001, **** p < 0.0001 versus LPS group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Phospho-proteomics, Activation Assay, Concentration Assay, CCK-8 Assay, Control, Western Blot, Membrane, Expressing

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: Inhibition of p38α MAPK alleviates oxidative stress in human colonic epithelial cells by activating the Nrf2 pathway. In the LPS-induced injury model of Ncm460 cells: (A,B) Representative flow cytometry scatter plots and quantitative analysis of intracellular ROS levels. (C) Levels of cellular oxidative stress markers (GSH, SOD, MDA). (D) Representative western blot images of Nrf2 and its downstream targets HO-1 and NQO1. The representative western blot images presented here are accompanied by the corresponding internal control detected on the same membrane. (E–G) Quantitative analysis of protein and mRNA expression levels of Nrf2 (E) , HO-1 (F) , and NQO1 (G) . n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus p38KD group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus LPS group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Inhibition, Flow Cytometry, Western Blot, Control, Membrane, Expressing

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: AKK enhances migration and tight junction integrity in human colonic epithelial cells in a p38α MAPK-dependent manner. In the LPS-induced injury model of Ncm460 cells: (A) Representative images and quantitative analysis of wound closure rate in the scratch assay. (B) Representative western blot images of tight junction proteins. The representative western blot images presented here are accompanied by the corresponding internal control detected on the same membrane. (C–E) Quantitative analysis of protein and mRNA expression levels of ZO-1 (C) , Occludin (D) , and Claudin-1 (E) . n = 6 independent biological replicates. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus p38KD group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus LPS group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Migration, Wound Healing Assay, Western Blot, Control, Membrane, Expressing

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: Akk restores the intestinal barrier by upregulating MUC2 and tight junction expression in a p38α MAPK-dependent manner. (A) Modulation of the mucus barrier by Akk and the p38α MAPK inhibitor (SB203580): representative IHC images of MUC2 and quantitative analysis. (B) Representative western blot images of tight junction proteins across groups. The representative western blot images presented here are accompanied by the corresponding internal control detected on the same membrane. (C–E) Quantitative analysis of protein and mRNA expression levels of ZO-1 (C) , occludin (D) , and claudin-1 (E) . (F,G) Serum levels of intestinal barrier damage markers, DAO activity, and D-LA concentration. n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus NC group; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus NS + ABX/LPS group, + p < 0.05, ++ p < 0.01, +++ p < 0.01, +++ p < 0.001, +++ p < 0.0001 versus the AKK-treated group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Expressing, Western Blot, Control, Membrane, Activity Assay, Concentration Assay

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: AKK alleviates intestinal oxidative stress by activating the Nrf2 signaling pathway through inhibition of p38α MAPK. (A) Levels of oxidative stress markers in colonic tissue: GSH, SOD, and MDA (B) Representative western blot images of Nrf2 and its downstream targets, HO-1 and NQO1. The representative western blot images presented here are accompanied by the corresponding internal control detected on the same membrane. n = 6 independent biological replicates. (C–E) Quantitative analysis of protein and mRNA expression levels of Nrf2 (C) , HO-1 (D) , and NQO1 (E) . n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus NC group; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus NS + ABX/LPS group, + p < 0.05, ++ p < 0.01, +++ p < 0.01, +++ p < 0.001, +++ p < 0.0001 versus the A-treated group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Inhibition, Western Blot, Control, Membrane, Expressing

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: Molecular docking predicts direct binding of AKK to p38α MAPK and validation in a murine model. Exploratory molecular docking results demonstrating strong binding between AKK and p38α MAPK: (A) Detailed view of the binding mode, with a binding free energy of −7.0 kcal·mol −1 ; (B) 3D representation of binding site interactions (yellow dashed lines indicate hydrogen bonds); (C) Schematic 3D structure of the complex; (D) 2D diagram of binding site interactions. (E) Top ten ranked binding conformations from docking screening. (F–I) Experimental validation in an ABX/LPS-induced mouse intestinal injury model: (F) Representative western blot images of p38α MAPK and p-p38α MAPK in colonic tissue; Blots for p38α MAPK and p-p38α MAPK were obtained from the same membrane. (G) p38α MAPK mRNA expression levels in the colon; (H) p-p38α MAPK/p38α MAPK ratio; (I) Total p-p38α MAPK protein levels. n = 6 independent biological replicates. All data are presented as mean ± SEM. # p < 0.05, ### p < 0.001, #### p < 0.0001 versus NC group; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus NS + ABX/LPS group, + p < 0.05, ++ p < 0.01, +++ < 0.01, +++ p < 0.001, +++ p < 0.0001 versus the AKK-treated group.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Binding Assay, Biomarker Discovery, Western Blot, Membrane, Expressing

Journal: Frontiers in Microbiology

Article Title: Akkermansia muciniphila alleviates antibiotic- and LPS-induced oxidative stress via the p38α MAPK–Nrf2 signaling axis

doi: 10.3389/fmicb.2026.1753421

Figure Lengend Snippet: A schematic model illustrating the role of the AKK-p38α MAPK-Nrf2 axis and microbial regulation in restoring intestinal homeostasis.

Article Snippet: Antibodies against p-p38α MAPK (#4511), HO-1(#43966), NQO-1(#3187) were purchased from Cell Signaling Technology (Danvers, MA, United States).

Techniques:

Journal: Antioxidants

Article Title: Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage

doi: 10.3390/antiox15020220

Figure Lengend Snippet: Sema3B increases HO-1 and TREM2 expression in perihematomal brain tissue and microglia after ICH. ( A – C ) Immunoblotting showing relative HO-1 and TREM2 protein expression in microglia under the different treatments ( n = 4). ( D , E ) Quantitative PCR (qRT-PCR) assessment of HO-1 and TREM2 transcript levels in microglia under the different treatments ( n = 3). ( F – H ) Protein analysis by Western blot for HO-1 and TREM2 in perihematomal tissue from ICH mice on post-ICH day 3 under the different treatments ( n = 4) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The antibodies used are as follows: Sema3B (1:2000, R&D Systems, USA), PlexinA1 (1:2000, Abcam, USA), Nrf2 (1:2000, Proteintech, Wuhan, China), TREM2 (1:2000, Proteintech, China), HO-1 (1:2000, Proteintech, China), PI3K (1:2000, Proteintech, China), phospho-PI3K (1:2000, Proteintech, China), AKT (1:2000, Proteintech, China), phospho-AKT (1:2000, Proteintech, China), SYK (1:2000, Proteintech, China), phospho-SYK (1:2000, Proteintech, China), mTOR (1:2000, Proteintech, China), phospho-mTOR (1:2000, Proteintech, China), p65 (1:2000, Proteintech, China), phospho-p65 (1:2000, Proteintech, China), IκB-α (1:2000, Proteintech, China), phospho-IκB-α (1:2000, Proteintech, China), CD206 (1:2000, Proteintech, China), CD86 (1:2000, Abclonal, China), DAP12 (1:2000, CST, Danvers, MA, USA), and GAPDH (1:3000, Proteintech, China).

Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Quantitative RT-PCR

Journal: Antioxidants

Article Title: Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage

doi: 10.3390/antiox15020220

Figure Lengend Snippet: Sema3B upregulates HO-1 and TREM2 expression via Nrf2. ( A , B ) Immunoblotting for relative Nrf2 protein expression in microglia under the different treatments ( n = 3). ( C ) Quantitative PCR (qRT-PCR) assessment of relative Nrf2 transcript levels in microglia under the different treatments ( n = 3). ( D ) Confocal micrographs depicting Nrf2 expression in microglia under the different treatments ( n = 3; scale bar = 10 μm). ( E – G ) Protein analysis by Western blot for HO-1 and TREM2 in microglia under the different treatments ( n = 3) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The antibodies used are as follows: Sema3B (1:2000, R&D Systems, USA), PlexinA1 (1:2000, Abcam, USA), Nrf2 (1:2000, Proteintech, Wuhan, China), TREM2 (1:2000, Proteintech, China), HO-1 (1:2000, Proteintech, China), PI3K (1:2000, Proteintech, China), phospho-PI3K (1:2000, Proteintech, China), AKT (1:2000, Proteintech, China), phospho-AKT (1:2000, Proteintech, China), SYK (1:2000, Proteintech, China), phospho-SYK (1:2000, Proteintech, China), mTOR (1:2000, Proteintech, China), phospho-mTOR (1:2000, Proteintech, China), p65 (1:2000, Proteintech, China), phospho-p65 (1:2000, Proteintech, China), IκB-α (1:2000, Proteintech, China), phospho-IκB-α (1:2000, Proteintech, China), CD206 (1:2000, Proteintech, China), CD86 (1:2000, Abclonal, China), DAP12 (1:2000, CST, Danvers, MA, USA), and GAPDH (1:3000, Proteintech, China).

Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Quantitative RT-PCR

Journal: Antioxidants

Article Title: Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage

doi: 10.3390/antiox15020220

Figure Lengend Snippet: Sema3B promotes hematoma absorption after ICH by enhancing PlexinA1-mediated microglial phagocytic function. Exogenous supplementation of Sema3B binds to its receptor PlexinA1, activating the DAP12-dependent signaling pathway (Syk-PI3K-AKT-mTOR) and NRF2 in microglia, thereby increasing the expression of TREM2 and HO-1 to facilitate microglia-mediated hematoma clearance, while suppressing neuroinflammation by inhibiting the NF-κB pathway and reducing pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). This figure was drawn by Figdraw.

Article Snippet: The antibodies used are as follows: Sema3B (1:2000, R&D Systems, USA), PlexinA1 (1:2000, Abcam, USA), Nrf2 (1:2000, Proteintech, Wuhan, China), TREM2 (1:2000, Proteintech, China), HO-1 (1:2000, Proteintech, China), PI3K (1:2000, Proteintech, China), phospho-PI3K (1:2000, Proteintech, China), AKT (1:2000, Proteintech, China), phospho-AKT (1:2000, Proteintech, China), SYK (1:2000, Proteintech, China), phospho-SYK (1:2000, Proteintech, China), mTOR (1:2000, Proteintech, China), phospho-mTOR (1:2000, Proteintech, China), p65 (1:2000, Proteintech, China), phospho-p65 (1:2000, Proteintech, China), IκB-α (1:2000, Proteintech, China), phospho-IκB-α (1:2000, Proteintech, China), CD206 (1:2000, Proteintech, China), CD86 (1:2000, Abclonal, China), DAP12 (1:2000, CST, Danvers, MA, USA), and GAPDH (1:3000, Proteintech, China).

Techniques: Expressing