ArticleBMC nephrology2025
Dioscin attenuates Gd-IgA1 overproduction by inhibiting the IL-6-JAK2/STAT3 signaling axis in IgA nephropathy.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy.Diagnostics (Basel, Switzerland) · 2026Review
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6 authors.
Funding
Abstract
backgroundInflammation is a key driver in IgA nephropathy (IgAN) pathogenesis. Recent studies have demonstrated a significant association between pro-inflammatory cytokine–triggered inflammatory cascades, particularly those involving interleukin-6 (IL-6), and disease progression in IgAN. However, the underlying molecular mechanisms remain to be fully elucidated. Dioscin (DIO), a major active compound in Yiqi Qingjie Formula— a standardized formula for IgAN treatment at Guang’anmen Hospital—has shown well-defined anti-inflammatory and immunomodulatory properties.
methodsPeripheral blood mononuclear cells (PBMCs) were isolated from 68 patients with IgA nephropathy (IgAN) and 16 healthy controls to assess key components of the IL-6 signaling pathway. An IgAN mouse model was established to evaluate the therapeutic effects of dioscin (DIO) and its potential anti-inflammatory mechanisms. The findings were further validated through complementary in vitro experiments.
resultsWe observed aberrant activation of the IL-6-mediated STAT3 signaling pathway in patients with IgAN. In vitro experiments further confirmed that IL-6 promoted the secretion of galactose-deficient IgA1 (Gd-IgA1) by activating the JAK2/STAT3 axis, which downregulated the expression of the key glycosyltransferases Core 1 β1,3-galactosyltransferase (C1GalT1) and Core 1 β3GalT-specific molecular chaperone (Cosmc). Importantly, DIO significantly inhibited JAK2/STAT3 phosphorylation in IgAN model mice, a finding that was validated again in vitro.
conclusionThis study shows that DIO reduces Gd-IgA1 production and alleviates renal injury by targeting and suppressing the IL-6-JAK2/STAT3 signaling pathway, offering a promising therapeutic strategy for IgAN.
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