Hyperoside alleviates adriamycin-induced podocyte injury via inhibiting mitochondrial fission
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Zhuyun Chen1,*, Xiaofei An2,*, Xi Liu1,*, Jia Qi3, Dafa Ding4, Min Zhao5, Suyan Duan1, Zhimin Huang1, Chengning Zhang1, Lin Wu1, Bo Zhang1, Aihua Zhang5, Yanggang Yuan1 and Changying Xing1
1Department of Nephrology, The First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China
2Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China
3Department of Pharmacy, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China
4Department of Endocrinology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China
5Department of Nephrology, Nanjing Children’s Hospital, Nanjing Medical University, Nanjing, China
*These authors have contributed equally to this work
Yanggang Yuan, email: email@example.com
Changying Xing, email: firstname.lastname@example.org
Keywords: hyperoside, adriamycin, mitochondrial fission, podocyte injury
Received: July 12, 2017 Accepted: August 27, 2017 Published: September 28, 2017
Podocyte injury underlies many forms of glomerular diseases. Our previous study showed that hyperoside, a naturally occurring flavonoid, could decrease albuminuria at the early stage of diabetic nephropathy by ameliorating renal damage and podocyte injury. However, its protective mechanism against podocyte injury is unknown. A previous study demonstrated that hyperoside might inhibit amyloid β-protein-induced neurotoxicity by suppressing mitochondrial dysfunction. Both mitochondrial dysfunction and its upstream determinant mitochondrial fission were closely related to podocyte injury. Thus, in the current study, we tested the effect of hyperoside on mitochondrial dysfunction and mitochondrial fission in adriamycin (ADR)-induced podocyte injury. In the mice model of ADR-induced nephropathy, hyperoside treatment inhibited ADR-induced albuminuria and podocyte injury. Meanwhile, hyperoside also blocked ADR-induced mitochondrial dysfunction and mitochondrial fission. Consistently, in cultured human podocytes, hyperoside suppressed ADR-induced podocyte injury, mitochondrial dysfunction and mitochondrial fission. All these results indicated that hyperoside might inhibit ADR-induced mitochondrial dysfunction and podocyte injury through suppressing mitochondrial fission both in vivo and in vitro. The underlying mechanisms which we revealed support the therapeutic effects of hyperoside for a broad range of glomerular diseases.
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