Renal failure · 2026
Soy protein alleviates DKD by restraining inflammation via the MAPKs/PPAR-γ signaling pathway.
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Zhang Ying, Xie Jing, Wang Minhui
Аннотация
BACKGROUND: Diabetic Kidney Disease (DKD), a leading cause of kidney failure driven by chronic inflammation and dysregulated signaling, lacks effective therapies. This study explored if soy protein alleviates DKD via the MAPKs/PPAR-γ pathway.
METHODS: Bioinformatics on GEO datasets (GSE154881, GSE139317) identified differentially expressed genes (DEGs): GSE154881 (peripheral blood) had 580 DEGs enriched in inflammation/MAPK signaling; GSE139317 (kidney tissues) had 2830 DEGs enriched in fatty acid metabolism/PPAR signaling, suggesting MAPK-PPAR-γ crosstalk. Although soy isoflavones have been reported to modulate MAPK or PPAR-γ signaling in other diseases, whether soy protein affects this pathway crosstalk in DKD remains unknown. Based on the bioinformatic prediction, we hypothesized that soy protein ameliorates DKD by targeting the MAPKs/PPAR-γ axis.
RESULTS: In streptozotocin-induced DKD mice, soy protein (200-800mg/kg) dose-dependently reduced serum creatinine, blood urea nitrogen, blood glucose, tubular injury, kidney pro-inflammatory cytokines (MCP-1, IL-6, TNF-α), and reversed weight loss. In high glucose-stimulated HK-2 cells, genistein (soy isoflavone, 20-100μM) dose-dependently restored viability, reduced MDA (oxidative stress), increased GSH (antioxidant), and lowered cytokines. p38 MAPK agonist (diprovocim) or PPAR-γ antagonist (GW9662) abolished these effects.
CONCLUSION: Soy protein alleviates DKD via genistein, which inhibits p38 MAPK and activates PPAR-γ to reduce inflammation/oxidative stress, supporting soy-based DKD interventions.
METHODS: Bioinformatics on GEO datasets (GSE154881, GSE139317) identified differentially expressed genes (DEGs): GSE154881 (peripheral blood) had 580 DEGs enriched in inflammation/MAPK signaling; GSE139317 (kidney tissues) had 2830 DEGs enriched in fatty acid metabolism/PPAR signaling, suggesting MAPK-PPAR-γ crosstalk. Although soy isoflavones have been reported to modulate MAPK or PPAR-γ signaling in other diseases, whether soy protein affects this pathway crosstalk in DKD remains unknown. Based on the bioinformatic prediction, we hypothesized that soy protein ameliorates DKD by targeting the MAPKs/PPAR-γ axis.
RESULTS: In streptozotocin-induced DKD mice, soy protein (200-800mg/kg) dose-dependently reduced serum creatinine, blood urea nitrogen, blood glucose, tubular injury, kidney pro-inflammatory cytokines (MCP-1, IL-6, TNF-α), and reversed weight loss. In high glucose-stimulated HK-2 cells, genistein (soy isoflavone, 20-100μM) dose-dependently restored viability, reduced MDA (oxidative stress), increased GSH (antioxidant), and lowered cytokines. p38 MAPK agonist (diprovocim) or PPAR-γ antagonist (GW9662) abolished these effects.
CONCLUSION: Soy protein alleviates DKD via genistein, which inhibits p38 MAPK and activates PPAR-γ to reduce inflammation/oxidative stress, supporting soy-based DKD interventions.