Journal: iScience

Article Title: Topical application of urolithin A activates mitophagy and enhances mitochondrial function to promote skin longevity

doi: 10.1016/j.isci.2026.117646

Figure Lengend Snippet: UA beneficial impact on human keratinocytes and reconstituted human epidermis (A) Mitochondrial respiration (basal and maximal) assessed as oxygen consumption rate (OCR) in human dermal keratinocytes after 72 h of differentiation from young donor treated with DMSO for 24 h or the indicated dose of UA. ∗ p < 0.05 and ∗∗∗ p < 0.001 after one-way ANOVA. Error bars represent mean ± SEM. (B) TOMM20 immunostaining of skin epidermis in a human full-thickness skin model from an old donor treated with or without UA 1 μM for 25 days. Data expressed as antibody staining signal over imaging field. ∗ p < 0.05 and ∗∗∗∗ p < 0.0001 after unpaired t test one-way ANOVA. Error bars represent mean ± SEM. Scale bars, 50 μm. (C) Relative gene expression of PINK1 and PARK2 in reconstructed human epidermis (RHE). RHE tissues were moisturized for 24 h with or without 1% Mitopure, and relative expression levels of PINK1 and PARK2 were quantified. Statistical analysis was performed using one-way ANOVA (∗ p < 0.05; ∗∗ p < 0.01). Error bars represent mean ± SEM. (D) Interleukin 6 levels normalized to cell viability in keratinocytes. Keratinocytes were stimulated with a pro-inflammatory cytokine mix for 24 h then treated for an additional 24 h with either DMSO or 1 μM UA. IL-6 secretion was quantified and normalized to cell viability. Statistical analysis was performed using one-way ANOVA (∗∗∗∗ p < 0.0001). Error bars represent mean ± SEM. (E) p16 immunostaining in a human full-thickness skin model from an old donor treated with or without UA 1 μM for 25 days. Data expressed as antibody staining signal over imaging field. ∗∗∗∗ p < 0.0001 after unpaired t test. Error bars represent mean ± SEM. Scale bars, 50 μm. (F) Ki67 immunostaining in a human full-thickness skin model from an old donor treated with or without UA 1 μM for 25 days. Data expressed as number of Ki67 positive cells normalized over μm of dermal epidermal junction (count/μm) ∗∗∗∗ p < 0.0001 after unpaired t test. Error bars represent mean ± SEM. Scale bars, 50 μm. (G) Keratin 10 immunostaining in a human full-thickness skin model from an old donor treated with or without UA 1 μM for 25 days. Data expressed as fluorescence intensity over epidermis area. ∗∗∗∗ p < 0.0001 after unpaired t test. Error bars represent mean ± SEM. Scale bars, 50 μm.

Article Snippet: IL-6 ELISA Kit , Proteintech , Cat#KE10007.

Techniques: Immunostaining, Staining, Imaging, Gene Expression, Expressing, Analysis, Fluorescence

Journal: iScience

Article Title: Topical application of urolithin A activates mitophagy and enhances mitochondrial function to promote skin longevity

doi: 10.1016/j.isci.2026.117646

Figure Lengend Snippet:

Article Snippet: IL-6 ELISA Kit , Proteintech , Cat#KE10007.

Techniques: Binding Assay, Ex Vivo, Recombinant, Metals, Enzyme-linked Immunosorbent Assay, Reverse Transcription, Cell Viability Assay, Staining, DC Protein Assay, Gene Expression, Glass, Software, Imaging, Microscopy, Real-time Polymerase Chain Reaction

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: Schematic illustration of the role of SUR1 in ALI and the protective mechanism of glibenclamide TNF-α binds to its receptor (TNFR), activating the NF-κB pathway and promoting inflammation through increased transcription of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In parallel, TNF-α induces mitochondrial dysfunction and ROS production, leading to DNA strand breaks. In response to DNA damage, nuclear PARP1 is activated to recruit DNA repair enzymes, promoting cell survival. Left, SUR1 interacts with and sequesters PARP1, impairing DNA damage repair. Accumulated DNA damage amplifies ROS production and NF-κB activation, which in turn further increases the transcription of inflammatory cytokines. This creates a positive feedback loop that promotes epithelial cell apoptosis and inflammation, contributing to ALI progression. Right, glibenclamide binds to SUR1 and disrupts the SUR1-PARP1 interaction, releasing PARP1 to restore DNA damage repair. This intervention breaks the pathological feedback loop by reducing ROS production, NF-κB activation, and inflammatory cytokine expression, thereby suppressing apoptosis and inflammation in epithelial cells and ultimately protecting against ALI.

Article Snippet: Recombinant human IL-6 protein , ABclonal Biotechnology , Cat# RP00201.

Techniques: Activation Assay, Expressing

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet:

Article Snippet: Recombinant human IL-6 protein , ABclonal Biotechnology , Cat# RP00201.

Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis