Journal: bioRxiv

Article Title: Local albumin excess exacerbates Candida albicans-induced inflammasome activation linked with hyperinflammation during vulvovaginal candidiasis

doi: 10.64898/2026.01.22.700771

Figure Lengend Snippet: (A) Overview of NLRP3 inflammasome priming and activation. DAMPs = damage-associated molecular patterns. TLR = Toll-like receptor. PAMPs = pathogen-associated molecular pattern. (B) IL-1β and IL-18 release by hMDMs ( n = 14 donors). (C) IL-1β release by mBMDMs ( n = 10). (D) IL-1β release by hMDMs in the presence of the inflammasome inhibitors KCl ( n = 8 donors) or VX-765 ( n = 9 donors). (E) Percentage ASC-positive mBMDMs ( n = 3 uninfected , n = 4 infected). (F, G) IL-1β release of mBMDMs deficient in the NLRP3 receptor ( Nlrp3 −/− ), the adapter proteins ASC ( Pycard −/− ) or the proteolytic enzyme caspase 1 ( Casp1 −/− / Casp11 −/− ) ( n = 4) or deficient in gasdermin D ( Gsdmd −/− ) (G). Bars represent the mean + SEM with dots as individual biological replicates: Individual donors (B, D) or mice (C, E - G) from at least three independently conducted experiments. Statistical significance was determined using a two-way ANOVA including with Holm-Šídák post-hoc test. * = P ≤ 0.05, ** = P ≤ 0.01, *** = P ≤ 0.001, **** = P ≤ 0.0001

Article Snippet: For inhibitor experiments, Anakinra (recombinant human IL-1Ra, 10 μg/mL, Kineret), potassium chloride (25 mM; Merck) or the caspase-1 inhibitor VX-765 (50 μg/mL; Invivogen) were added 1 h prior to infection.

Techniques: Activation Assay, Infection

Journal: Frontiers in Pharmacology

Article Title: Hyperoside ameliorates lupus nephritis by suppressing AKT1-mediated PANoptosis in podocytes: integrating network pharmacology and experimental validation

doi: 10.3389/fphar.2025.1726254

Figure Lengend Snippet: PANoptosis contributes to renal pathology in lupus nephritis. (A) Comparison of 24-h urinary protein levels between MRL/MpJ and MRL/lpr mice (n = 6). (B) Representative renal histology evaluated by H&E staining (n = 6). (C) TUNEL staining showing cell death in glomeruli (n = 6). (D) IHC analysis of podocyte markers (Podocalyxin, Nephrin, Synaptopodin, Podocin) in renal tissues. (E–G) Immunofluorescence staining of PANoptosis-related markers (NLRP3, RIPK3, Caspase-9) in kidney sections. (H) WB analysis of PANoptosis executor proteins (caspase-3, caspase-1, p-MLKL) in renal tissues, with bar graphs showing quantitative results relative to GAPDH (n = 3). (I) IF triple-staining of caspase-3, caspase-1, and p-MLKL in mouse kidney tissues. (J) Viability of MPC-5 cells treated with ICs at different concentrations and time points, measured by CCK-8 assay. (K) Flow cytometric analysis of cell death in MPC5 cells pretreated with VX-765 (10 μM), Nec-1 (20 μM), or Z-VAD (5 μM), followed by IC stimulation for 24 h. Bar graph shows the percentage of dead cells (n = 3). Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, ns: not significant.

Article Snippet: The inhibitors VX-765 (HY-13205), Necrostatin-1 (Nec-1, HY-15760), and Z-VAD-FMK (Z-VAD, HY-15760) were sourced from MedChemExpress (MCE, USA).

Techniques: Comparison, Staining, TUNEL Assay, Immunofluorescence, CCK-8 Assay