Salidroside ameliorates Adriamycin nephropathy in mice by inhibiting β‐catenin activity

• Published in: Journal of cellular and molecular medicine Vol. 23; no. 6; pp. 4443 - 4453
• Main Authors: Huang, Xinzhong, Xue, Haiyan, Ma, Jinyu, Zhang, Yunzhong, Zhang, Jing, Liu, Yue, Qin, Xiaogang, Sun, Cheng
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.06.2019; John Wiley and Sons Inc
• Subjects: Adriamycin nephropathy; Animals; Antibiotics, Antineoplastic - toxicity; beta Catenin - antagonists & inhibitors; Doxorubicin - toxicity; Gene Expression Regulation - drug effects; Glucosides - pharmacology; Kidney Diseases - chemically induced; Kidney Diseases - metabolism; Kidney Diseases - pathology; Kidney Diseases - prevention & control; Male; Mice; Mice, Inbred BALB C; Original; Phenols - pharmacology; podocytes; Podocytes - cytology; Podocytes - drug effects; Podocytes - metabolism; Proteinuria - etiology; Proteinuria - metabolism; Proteinuria - pathology; Proteinuria - prevention & control; salidroside; Signal Transduction; β‐catenin; β-catenin; salidroside; Adriamycin nephropathy; podocytes
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/jcmm.14340

Salidroside is a major phenylethanoid glycoside in Rhodiola rosea L., a traditional Chinese medicine, with multiple biological activities. It has been shown that salidroside possesses protective effects for alleviating diabetic renal dysfunction, contrast‐induced‐nephropathy and other kidney diseases. However, the involved molecular mechanism was still not understood well. Herein, we examined the protective effects of salidroside in mice with Adriamycin (ADR)‐induced nephropathy and the underlying molecular mechanism. The results showed that salidroside treatment ameliorates proteinuria; improves expressions of nephrin and podocin; and reduces kidney fibrosis and glomerulosclerosis induced by ADR. Mechanistically, ADR induces a robust accumulation of β‐catenin in the nucleus and stimulates its downstream target gene expression. The application of salidroside largely abolishes the nuclear translocation of β‐catenin and thus inhibits its activity. Furthermore, the activation of β‐catenin almost completely counteracts the protective roles of salidroside in ADR‐injured podocytes. Taken together, our data indicate that salidroside ameliorates proteinuria, renal fibrosis and podocyte injury in ADR nephropathy, which may rely on inhibition of β‐catenin signalling pathway.