ArticleJournal of diabetes research2026
Qiling Hushen Formula Ameliorates Type 2 Diabetic Kidney Disease via Gut-Kidney Axis Restoration and TLR4/NF-κB/NLRP3 Suppression.
Article in Journal of diabetes research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Qiling Hushen Formula Ameliorates Type 2 Diabetic Kidney Disease via Gut-Kidney Axis Restoration and TLR4/NF-κB/NLRP3 Suppression.Journal of diabetes research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
contextQiling Hushen Formula (QLHSF) has been widely used in clinical treatment for Type 2 diabetic kidney disease (T2DKD), yet its mechanism remains unclear.
objectiveThis study is aimed at elucidating the protective effects and mechanisms of QLHSF on T2DKD mice.
methodsChemical components of QLHSF were analyzed via ultraperformance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-QTOF-MS/MS). After 6 weeks of QLHSF intervention in C57BL/KSJ db/db mice, urine and serum samples were collected to measure biochemical parameters, inflammatory cytokines, and lipopolysaccharide (LPS) levels. Renal and colonic tissues were sectioned and subjected to histopathological staining. To evaluate the diversity and abundance of the gut microbiota, its composition was determined through 16S rRNA gene sequencing. Expression levels of colonic tight junction proteins, along with key proteins involved in the renal TLR4/NF-κB signaling pathway and NLRP3 inflammasome activation, were measured.
resultsQLHSF decreased proteinuria and improved renal function in T2DKD mice. Renal pathological injuries and intestinal barrier destruction were also alleviated. Analysis of 16S rRNA sequencing data demonstrated that QLHSF significantly modulated the gut microbiota composition, enriching beneficial bacteria such as g_Bacteroides, g_Lachnospiraceae_NK4A136_group, g_Alistipes, g_Muribaculum, g_Odoribacter, and g_Lachnoclostridium. QLHSF treatment led to a reduction in serum LPS levels and inhibition of the renal TLR4/NF-κB/NLRP3 signaling pathway, leading to reduced inflammatory cytokine production.
conclusionsIn T2DKD mice, QLHSF ameliorated proteinuria and renal injury through modulation of the gut microbiota, preservation of intestinal barrier integrity, and inhibition of the renal TLR4/NF-κB/NLRP3 pathway. These findings elucidate the pharmacological mechanism of QLHSF and provide strong experimental support for its clinical application in the treatment of T2DKD.
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.