European journal of nutrition · 2025
Xanthohumol exerts protective function on adriamycin-induced podocyte injury.
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Chen Huihui, Lin Hongzhou, Qian Rengcheng, Tang Guoqi, Ding Yinjuan, Jiang Yalan, Guo Xiaoling, Wang Dexuan
Аннотация
PURPOSE: Nephrotic syndrome (NS) is the main cause of the increasing end-stage renal disease (ESRD) patients worldwide. Podocytes are considered the crucial cells involved in the progression of NS, and their damage can directly lead to proteinuria. The objective of this study was to explore the protective effects of xanthohumol (XN) on podocyte injury.
METHODS: Adriamycin (ADR)-induced podocyte injury in vivo and in vitro models were established to explore the effects of XN on adriamycin nephropathy (AN) by urine and serum biochemical assay, periodic acid-schiff (PAS) staining, immunohistochemistry, immunofluorescence, western blot, and real-time quantitative PCR (RT-qPCR).
RESULTS: The results showed that XN could upregulate the expressions of podocyte specific marker Wilms' tumor protein 1 (Wt1), and glomerular filtration related functional proteins such as Nephrin, Synaptopodin, Zonula occludens 1 (ZO-1), and Crumbs2 (Crb2) as well as downregulate the expression of podocyte injury marker Desmin in ADR-treated podocytes to restrain the podocyte actin cytoskeleton disruption.
CONCLUSION: Our study showed that XN treatment significantly attenuated ADR-induced podocyte injury, suggesting that XN may be a potential therapy option for patients with NS.
METHODS: Adriamycin (ADR)-induced podocyte injury in vivo and in vitro models were established to explore the effects of XN on adriamycin nephropathy (AN) by urine and serum biochemical assay, periodic acid-schiff (PAS) staining, immunohistochemistry, immunofluorescence, western blot, and real-time quantitative PCR (RT-qPCR).
RESULTS: The results showed that XN could upregulate the expressions of podocyte specific marker Wilms' tumor protein 1 (Wt1), and glomerular filtration related functional proteins such as Nephrin, Synaptopodin, Zonula occludens 1 (ZO-1), and Crumbs2 (Crb2) as well as downregulate the expression of podocyte injury marker Desmin in ADR-treated podocytes to restrain the podocyte actin cytoskeleton disruption.
CONCLUSION: Our study showed that XN treatment significantly attenuated ADR-induced podocyte injury, suggesting that XN may be a potential therapy option for patients with NS.