Jieduquyuzishen Prescription Attenuates Renal Fibrosis in MRL/lpr Mice via Inhibiting EMT and TGF-β1/Smad2/3 Pathway

Author:

Wu Shan1ORCID,Ji Lina2,Fan Xuemin3,Fang Sijia4,Bao Jie5,Yuan Xiao6,Fan Yongsheng5,Xie Guanqun5ORCID

Affiliation:

1. Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, Zhejiang, China

2. The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, Zhejiang, China

3. Department of Medical Administration, Hangzhou Emergency Medical Center in Zhejiang Province, Hangzhou 310003, Zhejiang, China

4. Hangzhou TCM Hospital of Zhejiang Chinese Medical University, Hangzhou 310007, Zhejiang, China

5. School of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China

6. The Department of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, Zhejiang, China

Abstract

Jieduquyuziyin prescription (JP) has been used to treat lupus nephritis (LN) and its effectiveness in the treatment of LN has been clinically proven, but the underlying mechanisms have yet to be completely understood. This aim of this study was to clarify the efficacy of JP on the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells and the molecular mechanisms of JP in MRL/lpr mice. In vivo, we observed the therapeutic actions of JP in MRL/lpr mice as well as its antifibrosis effect and potential mechanism. In vitro, we evaluated the role of JP in EMT and its possible mechanism through the EMT of human renal proximal tubular epithelial cells (HK-2) induced by transforming growth factor-beta 1 (TGF-β1) and M2c macrophages. HK-2 cells were treated with JP-treated serum, and MRL/lpr mice were treated by JP for 8 weeks. The results showed that JP alleviated disease activity, improved renal function, decreased proteinuria, and improved renal injury and fibrosis in MRL/lpr mice. Furthermore, JP suppressed the activation of the TGF-β1/Smad2/3 signaling pathway, upregulated the E-cadherin levels, and downregulated the Vimentin and mesenchymal α-smooth muscle actin (α-SMA) levels in the kidney of MRL/lpr mice. JP was further found to prevent the TGF-β1 and M2c macrophages-induced EMT of HK-2 cells. Collectively, JP could alleviate the disease activity of MRL/lpr mice, improve renal function, and attenuate renal fibrosis, and its underlying mechanisms may be related to the inhibition of EMT and TGF-β1/Smad2/3 signaling pathway.

Funder

Natural Science Foundation of Zhejiang Province

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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