Open Access

Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction

  • Authors:
    • Long Zheng
    • Chao Zhang
    • Long Li
    • Chao Hu
    • Mushuang Hu
    • Niyazi Sidikejiang
    • Xuanchuan Wang
    • Miao Lin
    • Ruiming Rong
  • View Affiliations

  • Published online on: February 16, 2017     https://doi.org/10.3892/mmr.2017.6208
  • Pages: 1702-1712
  • Copyright: © Zheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have demonstrated the potential antifibrotic effects of baicalin in vitro, via examination of 21 compounds isolated from plants. However, its biological activity and underlying mechanisms of action in vivo remain to be elucidated. The present study aimed to evaluate the effect of baicalin on renal fibrosis in vivo, and the potential signaling pathways involved. A unilateral ureteral obstruction (UUO)‑induced renal fibrosis model was established using Sprague‑Dawley rats. Baicalin was administrated intraperitoneally every 2 days for 10 days. The degree of renal damage and fibrosis was investigated by histological assessment, and detection of fibronectin and collagen I mRNA expression levels. Epithelial‑mesenchymal transition (EMT) markers, transforming growth factor-β1 (TGF-β1) levels and downstream phosphorylation of mothers against decapentaplegic 2/3 (Smad2/3) were examined in vivo and in an NRK‑52E rat renal tubular cell line in vitro. Baicalin was demonstrated to markedly ameliorate renal fibrosis and suppress EMT, as evidenced by reduced interstitial collagen accumulation, decreased fibronectin and collagen I mRNA expression levels, upregulation of N‑ and E‑cadherin expression levels, and downregulation of α‑smooth muscle actin and vimentin expression. Furthermore, baicalin decreased TGF‑β1 expression levels in serum and kidney tissue following UUO, and suppressed Smad2/3 phosphorylation in rat kidney tissue. In vitro studies identified that baicalin may inhibit the phosphorylation of Smad2/3 under the same TGF‑β1 concentration. In conclusion, baicalin may protect against renal fibrosis, potentially via inhibition of TGF‑β1 production and its downstream signal transduction.
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April-2017
Volume 15 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Zheng L, Zhang C, Li L, Hu C, Hu M, Sidikejiang N, Wang X, Lin M and Rong R: Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction. Mol Med Rep 15: 1702-1712, 2017
APA
Zheng, L., Zhang, C., Li, L., Hu, C., Hu, M., Sidikejiang, N. ... Rong, R. (2017). Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction. Molecular Medicine Reports, 15, 1702-1712. https://doi.org/10.3892/mmr.2017.6208
MLA
Zheng, L., Zhang, C., Li, L., Hu, C., Hu, M., Sidikejiang, N., Wang, X., Lin, M., Rong, R."Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction". Molecular Medicine Reports 15.4 (2017): 1702-1712.
Chicago
Zheng, L., Zhang, C., Li, L., Hu, C., Hu, M., Sidikejiang, N., Wang, X., Lin, M., Rong, R."Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction". Molecular Medicine Reports 15, no. 4 (2017): 1702-1712. https://doi.org/10.3892/mmr.2017.6208