Journal: Oxidative Medicine and Cellular Longevity

Article Title: Sodium Butyrate Ameliorates Oxidative Stress-Induced Intestinal Epithelium Barrier Injury and Mitochondrial Damage through AMPK-Mitophagy Pathway

doi: 10.1155/2022/3745135

Figure Lengend Snippet: Effects of sodium butyrate (NaB) on oxidative stress, intestinal epithelium barrier, and mitophagy of porcine intestinal epithelial cells (IPEC-J2) after inhibiting mitophagy or AMPK. (a–c) Superoxide dismutase (SOD), glutathione reductase (GSH) activity, and malondialdehyde (MDA) content of IPEC-J2 treated with Mdivi-1 or Compound C (CC). (d) Cellular mitochondrial membrane potential quantification by flow cytometry. (e) Cellular reactive oxygen species (ROS) level quantification by flow cytometry. (f) Intestinal epithelial transepithelial resistance (TER) and fluorescein isothiocyanate dextran 4 kDa (FD4) permeability. (g) Protein expression and quantification of tight junction Claudin-1, Occludin, and ZO-1. ∗ indicates a significant difference compared with the control group ( P < 0.05); # indicates a significant difference compared with the H2O2 group ( P < 0.05); & indicates a significant difference compared with the NaB+H2O2 group ( P < 0.05).

Article Snippet: Trypsin (Beyotime Biotechnology, China), phosphate-buffered saline (PBS) (Bozan Biotechnology, China), penicillin-streptomycin (Solabao Biotechnology, China), fetal bovine serum (Gemini, Australia), CCK-8 kit (Beyotime Biotechnology, China), MitoSpyTM Red CMXRos (Biolegend, USA), immunofluorescence fixative (Sevier Biotechnology, China), Triton-X 100 (Sigma-Aldrich, St. Louis, MO, USA), Glycine (Sinopharm Group, China), DAPI (Beyotime Biotechnology, China), Goat Anti-Mouse IgG Dylight 594 (Earthox, USA), Goat Anti-Mouse IgG Dylight 488 (Earthox, USA), mitochondrial division inhibitor (Mdivi-1) (Selleck, USA), AMPK inhibitor (Compound C, CC) (Selleck, USA), Lipofectamine RNAiMAX, and Lipofectamine 2000 were obtained from Invitrogen (Invitrogen, USA).

Techniques: Activity Assay, Membrane, Flow Cytometry, Permeability, Expressing, Control

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Sodium Butyrate Ameliorates Oxidative Stress-Induced Intestinal Epithelium Barrier Injury and Mitochondrial Damage through AMPK-Mitophagy Pathway

doi: 10.1155/2022/3745135

Figure Lengend Snippet: Effects of sodium butyrate (NaB) on mitophagy, oxidative stress, and intestinal epithelium barrier after interference with AMPK α . (a) Expression and quantification of mitophagy proteins PINK1, Parkin, and P62. (b–d) Superoxide dismutase (SOD), glutathione reductase (GSH) activity, and malondialdehyde (MDA) content of porcine intestinal epithelial cells (IPEC-J2). (e) Cellular reactive oxygen species (ROS) level of IPEC-J2. (f) Cellular mitochondrial membrane potential of IPEC-J2. (g) Protein expression and quantification of recombinant NLR family, pyrin domain-containing protein 3 (NLRP3) and Caspase-1. (h) Intestinal epithelial transepithelial resistance (TER) and fluorescein isothiocyanate dextran 4 kDa (FD4) permeability. ∗ indicates a significant difference compared with the control group ( P < 0.05).

Article Snippet: Trypsin (Beyotime Biotechnology, China), phosphate-buffered saline (PBS) (Bozan Biotechnology, China), penicillin-streptomycin (Solabao Biotechnology, China), fetal bovine serum (Gemini, Australia), CCK-8 kit (Beyotime Biotechnology, China), MitoSpyTM Red CMXRos (Biolegend, USA), immunofluorescence fixative (Sevier Biotechnology, China), Triton-X 100 (Sigma-Aldrich, St. Louis, MO, USA), Glycine (Sinopharm Group, China), DAPI (Beyotime Biotechnology, China), Goat Anti-Mouse IgG Dylight 594 (Earthox, USA), Goat Anti-Mouse IgG Dylight 488 (Earthox, USA), mitochondrial division inhibitor (Mdivi-1) (Selleck, USA), AMPK inhibitor (Compound C, CC) (Selleck, USA), Lipofectamine RNAiMAX, and Lipofectamine 2000 were obtained from Invitrogen (Invitrogen, USA).

Techniques: Expressing, Activity Assay, Membrane, Recombinant, Permeability, Control

Journal: American Journal of Translational Research

Article Title: The roles of AMPK-mediated autophagy and mitochondrial autophagy in a mouse model of imiquimod-induced psoriasis

doi:

Figure Lengend Snippet: Effects of AMPK modulation on the mRNA expression of autophagy and mitochondrially associated proteins. The sequences of the forward and reverse primers for Atg7, P62, PINK1, and Parkin (A). The mRNA expression levels of Atg7 (B), P62 (C), PINK1 (D), and Parkin (E) in the skin after back injury in the psoriasis mouse model. Statistical analysis was conducted with one-way ANOVA, then with a Student-Newman-Keuls post hoc test. There were n=6 animals per group. Data are expressed as the mean ± SD. *P<0.05, **P<0.01, ***P<0.001, compared with the control group. #P<0.05, ##P<0.01, ###P<0.001, compared with the IMQ + vehicle group.

Article Snippet: In the IMQ + CC group, the AMPK inhibitor CC (Cayman, USA, 10 mg/kg) was intraperitoneally injected once per day for 8 consecutive days.

Techniques: Expressing, Control

Journal: American Journal of Translational Research

Article Title: The roles of AMPK-mediated autophagy and mitochondrial autophagy in a mouse model of imiquimod-induced psoriasis

doi:

Figure Lengend Snippet: Expression levels of autophagy-associated proteins in mice after AMPK modulation. The protein-expression levels of AMPK and p-AMPK (A, B), ULK1 and p-ULK1 (C, D), Atg7 (E, F), and P62 (G, H) were assessed to determine the effects of AMPK modulation on back skin injury in a psoriasis mouse model. Statistical analysis was conducted with one-way ANOVA, then with a Student-Newman-Keuls post hoc test. There were n=6 animals per group. Data are expressed as the mean ± SD. *P<0.05, **P<0.01, ***P<0.001, compared with the control group. #P<0.05, ###P<0.001, compared with the IMQ + vehicle group.

Article Snippet: In the IMQ + CC group, the AMPK inhibitor CC (Cayman, USA, 10 mg/kg) was intraperitoneally injected once per day for 8 consecutive days.

Techniques: Expressing, Control

Journal: American Journal of Translational Research

Article Title: The roles of AMPK-mediated autophagy and mitochondrial autophagy in a mouse model of imiquimod-induced psoriasis

doi:

Figure Lengend Snippet: Expression levels of mitophagy-associated proteins in mice after AMPK modulation. The protein-expression levels of PINK1 (A, B), Parkin (C, D), and LC3 (E, F) were evaluated to determine the effect of AMPK modulation on autophagy in a psoriasis mouse model. Statistical analysis was conducted with one-way ANOVA, then with a Student-Newman-Keuls post hoc test. There were n=6 animals per group. Data are expressed as the mean ± SD. **P<0.01, ***P<0.001, compared with the control group. ##P<0.01, ###P<0.001, compared with the IMQ + vehicle group.

Article Snippet: In the IMQ + CC group, the AMPK inhibitor CC (Cayman, USA, 10 mg/kg) was intraperitoneally injected once per day for 8 consecutive days.

Techniques: Expressing, Control