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黄腐酚对阿霉素诱导的足细胞损伤具有保护作用。

Xanthohumol exerts protective function on adriamycin-induced podocyte injury.

作者信息

Chen Huihui, Lin Hongzhou, Qian Rengcheng, Tang Guoqi, Ding Yinjuan, Jiang Yalan, Guo Xiaoling, Wang Dexuan

机构信息

Department of Pediatrics, The Second School of Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Key Laboratory of Structural Malformations in Children of Zhejiang Province, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

出版信息

Eur J Nutr. 2025 Sep 18;64(6):278. doi: 10.1007/s00394-025-03799-3.

Abstract

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.

摘要

目的

肾病综合征(NS)是全球范围内终末期肾病(ESRD)患者数量增加的主要原因。足细胞被认为是参与NS进展的关键细胞,其损伤可直接导致蛋白尿。本研究的目的是探讨黄腐酚(XN)对足细胞损伤的保护作用。

方法

建立阿霉素(ADR)诱导的足细胞损伤体内和体外模型,通过尿液和血清生化检测、高碘酸-希夫(PAS)染色、免疫组织化学、免疫荧光、蛋白质印迹法和实时定量聚合酶链反应(RT-qPCR)来探讨XN对阿霉素肾病(AN)的影响。

结果

结果表明,XN可上调足细胞特异性标志物威尔姆斯瘤蛋白1(Wt1)以及肾小球滤过相关功能蛋白如Nephrin、Synaptopodin、紧密连接蛋白1(ZO-1)和Crb2的表达,并下调阿霉素处理的足细胞中足细胞损伤标志物结蛋白的表达,以抑制足细胞肌动蛋白细胞骨架的破坏。

结论

我们的研究表明,XN治疗可显著减轻ADR诱导的足细胞损伤,提示XN可能是NS患者的一种潜在治疗选择。

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