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Sulforaphane alleviates membranous nephropathy by inhibiting oxidative stress-associated podocyte pyroptosis
Daoyuan Lv1,2, Laping Chu1,2, Yuan Du1,2
1Department of Nephrology, Affiliated Hospital of Jiangnan University, Wuxi, China.
Objectives:
To investigate the natural product sulforaphane (SFN) in protection of membranous nephropathy (MN) by inhibiting oxidative stress-associated podocyte pyroptosis.
Materials And Methods:
A passive Heymann nephritis (PHN) model was established and treated with SFN. Clinical manifestations were examined by testing 24-hr urine protein, albumin, total cholesterol, triglyceride, high-density and low-density lipoprotein levels. Podocyte injury was observed through glomerular ultrastructure and the expression of podocin and desmin. Intrarenal oxidative stress was evaluated through assessment of oxidative markers, including malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine, and the activities of anti-oxidant enzymes, including total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. Podocyte and intrarenal pyroptosis were investigated by observing the localization of the GSDMD N-terminus (GSDMD(N)) in podocytes; the expression of pyroptosis signaling pathway, including GSDMD, NF-κB p65, p-NF-κB p65 (Ser536), NLRP3, ASC, caspase-1, IL-1β, and IL-18; and pyroptosis encounter Nrf2 in the glomeruli and kidney.
Results:
SFN has a protective effect on MN, as reflected by alleviation of nephrotic syndrome, amelioration of podocyte foot process fusion, increased expression and normalization of podocin, and decreased expression of desmin in the glomeruli. Mechanistically, SFN relieved intrarenal oxidative stress, as indicated by decreased renal malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine and increased activity of total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. SFN also inhibited podocyte and intrarenal pyroptosis, as revealed by decreased colocalization of GSDMD (N) with synaptopodin and ZO-1, decreased expression of pyroptosis signaling pathway, and increased expression of Nrf2 in the glomeruli and kidney.
Conclusion:
SFN could alleviate MN by inhibiting oxidative stress-associated podocyte pyroptosis.
Insights
Sulforaphane (SFN) protects against membranous nephropathy (MN) by reducing oxidative stress and pyroptosis in podocytes. This natural compound alleviates kidney damage and offers a potential therapeutic strategy for MN.
Area of Science:
- Nephrology
- Molecular Biology
- Natural Products Chemistry
Background:
- Membranous nephropathy (MN) is a leading cause of nephrotic syndrome.
- Podocyte injury and pyroptosis are key pathological mechanisms in MN.
- Oxidative stress exacerbates podocyte damage in kidney diseases.
Purpose of the Study:
- To investigate the protective effects of sulforaphane (SFN) against membranous nephropathy (MN).
- To elucidate the role of SFN in inhibiting oxidative stress-associated podocyte pyroptosis in MN.
Main Methods:
- A passive Heymann nephritis (PHN) rat model was utilized.
- Treatment with SFN was administered to assess clinical and pathological changes.
- Oxidative stress markers, antioxidant enzyme activities, and pyroptosis signaling pathways were analyzed.
Main Results:
- SFN treatment alleviated nephrotic syndrome and ameliorated podocyte injury in the PHN model.
- SFN significantly reduced intrarenal oxidative stress markers and enhanced antioxidant enzyme activity.
- SFN inhibited podocyte and intrarenal pyroptosis by downregulating key signaling molecules.
Conclusions:
- Sulforaphane demonstrates significant protective effects against membranous nephropathy.
- SFN alleviates MN by mitigating oxidative stress and inhibiting pyroptosis in podocytes.
- SFN represents a promising therapeutic agent for managing membranous nephropathy.
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