Source: openalex · Origin: CN · Qingyue Meng, Bo Chen, Chunjiang Zhang, Lin Jia, Xingyu Yao · PubMed · 2026-06-01
URL: https://doi.org/10.14670/hh-25-021
AI rationale (4/5, tier: preliminary): In-vitro mechanistic study directly targeting NLRP3 inflammasome and ROS/TXNIP pathway in metabolic disease context, but lacks human biomarkers or clinical translation.
BACKGROUND: in diabetic nephropathy (DN) progression and its underlying mechanism targeting the ROS/TXNIP/NLRP3 inflammasome pathway. METHODS: (1-50 nM), or high glucose plus N-acetylcysteine (NAC, 10 mM). Cell viability was assessed by the CCK-8 assay. Oxidative stress parameters (ROS via DCFH-DA fluorescence, MDA content, SOD activity) and pyroptosis markers (LDH release, PI/Hoechst 33342 nuclear staining) were quantified. Renal histopathology was performed using PAS and Masson trichrome staining. Biochemical analyses included serum creatinine, urea nitrogen, and 24-h urinary protein quantification. Molecular profiling encompassed ELISA (IL-1β, IL-6, TNF-α, IL-18, fibronectin, collagen IV), RT-qPCR (NOX2, NOX4, NLRP3, ASC), western blotting (TXNIP, NLRP3, ASC, caspase-1, IL-1β, IL-18, collagen IV, fibronectin, laminin), and TXNIP immunofluorescence. RESULTS: suppressed ROS/TXNIP/NLRP3/caspase-1 signaling, ameliorated renal dysfunction, and mitigated histopathological damage in DN rats. CONCLUSION: confers renoprotection in DN by inhibiting the ROS/TXNIP/NLRP3 inflammasome axis, thereby suppressing oxidative stress, inflammatory cytokine production, ECM accumulation, and pyroptotic cell death in glomerular mesangial cells and renal tissues.