ArticleScientific reports2025
Capilliposide A attenuates diabetic nephropathy via modulation of NF-κB/TLR4 and apoptotic pathways.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
This study aimed to identify therapeutic targets and signaling pathways of Capilliposide A (LC-A) for diabetic nephropathy (DN) through integrated network pharmacology and experimental validation. Using a DN mouse model induced by high-fat diet (HFD) and streptozotocin (STZ), we investigated the molecular mechanisms of LC-A. The PubChem database provided the two-dimensional structure of LC-A, with subsequent identification of LC-A/DN-associated targets through intersection analysis. Core targets were determined via protein-protein interaction (PPI) network construction, followed by gene ontology enrichment and pathway analyses. Molecular docking simulations evaluated LC-A's binding affinity to DN-related targets. C57BL/6 mice receiving HFD and STZ intraperitoneal injections were treated daily with LC-A or metformin (MET) via oral gavage for 8 weeks. Weekly monitoring included body weight and blood glucose measurements. Post-treatment assessments encompassed serum lipid profiles, renal function biomarkers, inflammatory cytokines, oxidative stress markers, and renal histopathology. Western blotting, immunohistochemistry, and immunofluorescence were performed to analyze inflammatory pathway proteins and apoptosis-related factors. Network pharmacology identified TLR4, NF-κB1, STAT3, EGFR, mTOR, and MAPK as core targets involved in inflammation, oxidative stress, and apoptosis regulation. Pathway enrichment analysis revealed critical inflammatory pathways including IL-17, TNF, and Th17 cell differentiation. Molecular docking confirmed stable binding of LC-A to TLR4, NF-κB1, Bax, and Bcl-2. In vivo experiments demonstrated that LC-A significantly reduced renal injury markers (KI, SCR, BUN), lipid profiles (TG, TC), and oxidative stress (MDA), while enhancing antioxidant enzymes (SOD, GPX, CAT) in DN mice (P < 0.05). LC-A effectively suppressed serum inflammatory cytokines (IL-6, TNF-α, IL-1β, MCP-1, iNOS) through NF-κB pathway modulation and apoptosis regulation (P < 0.05). Histopathological analysis revealed attenuated renal cortical vacuolization, tubular swelling, glomerular mesangial expansion, sclerosis, and inflammatory infiltration. These findings suggest LC-A as a promising natural nephroprotective agent for DN prevention and treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.