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Research articles

ScienceAsia 47 (2021): 293-302 |doi: 10.2306/scienceasia1513-1874.2021.034

Acteoside ameliorates diabetic kidney disease via regulating the activation of the PPARγ/β-catenin pathway

Yi-Hua Bai, Min Yang*, Zhi-Jian Feng, Shuai Zheng

ABSTRACT:     Diabetic kidney disease (DKD) is a common complication of diabetes. Acteoside is the main component of Rehmannia glutinosa leaves that shows renal protective effects. This study aimed to explore the protective role of acteoside on podocytes in DKD. Mouse podocyte cell line MPC-5 was stimulated with advanced glycation end products (AGEs) to establish an in vitro DKD model and, then, treated with or without acteoside. The expression levels of miR-27a, PPAR (peroxisome proliferator-activated receptor), and β-catenin were measured at 24 h and 48 h posttreatment. Sprague-Dawley rats were randomly divided into 5 groups: control; DKD; A-1 (DKD + low dose acteoside); A-2 (DKD + medium dose acteoside); and A-3 (DKD + high dose acteoside). The blood and urine biochemical indexes and the renal expressions of miR-27a, PPAR-1γ, and β-catenin were detected. Compared with the control group, the expressions of α-SMA, Snail-1, miR-27a, and β-catenin in AGE-stimulated cells were significantly higher. The effects of acteoside intervention significantly downregulated their expression in AGE-challenged group. The levels of PPARγ and synaptopodin in AGE-stimulated cells were significantly lower than those in the control group, whereas acteoside treatment significantly restored the expressions of these genes. Acteoside alleviated podocyte injury by downregulating miR-27a expression, rescuing the reduction of PPARγ, and inhibiting the activation of β-catenin signaling in the kidney tissues of DKD rats. Acteoside ameliorated podocyte injury in DKD by inhibiting the activation of PPARγ/β- catenin signaling pathway and this process might involve the regulation of miR-27a expression. Our findings suggest a therapeutic potential of acteoside in treating podocyte injury in DKD.

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a Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan 650101 China

* Corresponding author, E-mail: miny524036@163.com

Received 24 Mar 2020, Accepted 29 Jan 2021