| ORIGINAL ARTICLE |
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| Year : 2021 | Volume
: 8
| Issue : 1 | Page : 2 |
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Tangshen formula attenuates renal fibrosis by downregulating transforming growth factor β1/Smad3 and LncRNA-MEG3 in rats with diabetic kidney disease
Xue-Feng Zhou1, Ying Wang1, Min-Jing Luo1, Ting-Ting Zhao2, Ping Li2
1 Department of Clinical Medicine, Beijing University of Chinese Medicine; Department of Pharmacology, Beijing Key Laboratory for Immune-mediated Inflammatory Diseases, Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
2 Department of Pharmacology, Beijing Key Laboratory for Immune-mediated Inflammatory Diseases, Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China
Correspondence Address:
Prof. Ping Li
Department of Pharmacology,Beijing Key Laboratory for Immune-mediated Inflammatory Diseases, Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing
China
Prof. Ting-Ting Zhao
Department of Pharmacology,Beijing Key Laboratory for Immune-mediated Inflammatory Diseases, Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing
China
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/imna.imna_22_21
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Background and Objective: The traditional Chinese Tangshen formula (TSF) has been reported to ameliorate diabetic kidney disease (DKD) in humans and animals. However, the effect of TSF on renal fibrosis remains unclear. Transforming growth factor-β1 (TGF-β1)/Smad3 signaling and lncRNA MEG3 are important in renal fibrosis. In this study, we examined the therapeutic effect of TSF on renal fibrosis and explored whether it was related to the modulation of TGFβ1/Smad3 signaling and lncRNA MEG3 expression. Materials and Methods: Experiments were performed in rats in vivo and in the HK2 cells in vitro. DKD was induced in rats by uninephrectomy combined with a single streptozotocin injection. The HK2 cells were stimulated by high glucose (HG) to explore the mechanism of TSF effects in vitro. Results: TSF significantly attenuated renal injury by lowering proteinuria and renal histological damage in DKD rats. TSF reduced collagen deposition by decreasing the expression of the fibrotic indicators collagen I, collagen IV, and fibronectin at the protein and mRNA levels, which suggested that TSF ameliorated DKD by decreasing renal fibrosis. Furthermore, TSF decreased TGF-β1 expression and suppressed the levels of phosphorylated Smad3 and Smad2/3 in vivo. Moreover, TSF downregulated the lncRNA MEG3 level in DKD rats. TSF reversed the upregulation of collagen I and fibronectin expression and downregulated Smad2/3 phosphorylation in the HK2 cells stimulated with HG. Conclusions: TSF ameliorates renal fibrosis in rats with DKD by suppressing TGF-β1/Smad3 signaling and lncRNA MEG3 expression.
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