ArticleNutrients2026
Punicalagin Alleviates Diabetic Kidney Injury: Potential Involvement of SESN2-Related Mitophagy and Changes in Pyroptosis-/Ferroptosis-Related Indicators.
Article in Nutrients, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
objectivesDiabetic kidney disease (DKD) is a progressive nephropathy associated with excessive pyroptosis and ferroptosis. Impaired renal mitophagy has been implicated in inflammation and lipid peroxidation in DKD; however, it remains unclear whether and how it modulates pyroptosis and ferroptosis. Punicalagin (PU), a natural polyphenol with potent anti-inflammatory and antioxidant activities, has been shown to improve DKD, yet its underlying mechanism requires further elucidation. This study aimed to investigate whether PU alleviates pyroptosis- and ferroptosis-related indicators in diabetes-associated renal injury in association with SESN2-related mitophagy, using both in vivo and in vitro models.
methodsWe established a diabetic mouse model using a high-fat diet and streptozotocin (STZ) injection. After successful modeling, we measured serum blood urea nitrogen (BUN) and creatinine (CREA), and stained renal tissues with HE, Masson, and PASM for pathological scoring. Protein expression of kidney injury molecule-1 (KIM-1), pyroptosis-related (caspase-1, IL-18), ferroptosis-related (FTH1, ACSL4), mitophagy-related (PINK1, Parkin, p62, LC3-II/I), and SESN2 were quantified by Western blotting. In high-glucose-induced HK-2 cells, glucose uptake was assessed by 2-NBDG, pyroptotic/ferroptotic morphology by electron microscopy, and TOM20/LC3 co-localization by confocal microscopy. Furthermore, Mitochondrial Division Inhibitor 1 (Mdivi-1) was used to probe the potential involvement of mitophagy in the effects of PU on pyroptosis- and ferroptosis-related markers, and transfection of
resultsDiabetic mice exhibited renal histological abnormalities, elevated BUN/CREA, and increased KIM-1 expression. Additionally, pyroptosis- and ferroptosis-related proteins were dysregulated, while mitophagy-related proteins and SESN2 were downregulated. PU treatment significantly reversed these abnormalities, which were confirmed in high-glucose-treated HK-2 cells. In the high-glucose-induced HK-2 cell model, treatment with Mdivi-1 attenuated the effects of PU on pyroptosis- and ferroptosis-related markers. In parallel, knockdown of
conclusionsPU may modulate mitophagy-related signaling in association with SESN2, accompanied by changes in pyroptosis- and ferroptosis-related markers in diabetes-associated renal injury. This study provides preliminary evidence for the renoprotective effect of PU against DKD, potentially involving SESN2-related mitophagy and the concurrent regulation of pyroptosis- and ferroptosis-related markers in renal cells. Collectively, PU warrants further investigation as a candidate compound for DKD.
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