4.6 Article

Anti-EMT and anti-fibrosis effects of protocatechuic aldehyde in renal proximal tubular cells and the unilateral ureteral obstruction animal model

期刊

PHARMACEUTICAL BIOLOGY
卷 60, 期 1, 页码 1198-1206

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/13880209.2022.2088809

关键词

Epithelial-mesenchymal transition; renal fibrosis; unilateral ureteral obstruction

资金

  1. Ministry of Science and Technology, Taiwan, Republic of China [MOST 106-2314-B-075A-012-MY2]

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This study evaluated the effects of protocatechuic aldehyde (PCA) on renal fibrosis. The results showed that PCA could inhibit TGF-beta 1-induced fibrosis and EMT, suggesting it as a potential strategy for preventing organ fibrosis in clinics.
Context Protocatechuic aldehyde (PCA) is a natural product that has various benefits for fibrosis. Objective This study evaluated the effects of PCA on renal fibrosis. Materials and methods Epithelial-mesenchymal transition (EMT) was induced by 20 ng/mL transforming growth factor-beta 1 (TGF-beta 1), followed by treatment with 1 and 5 mu M PCA, in the rat renal proximal tubular cell line NRK-52E. Cell viability, protein expression, and scratch wound-healing assays were conducted. Sprague-Dawley (SD) rats underwent unilateral ureteral obstruction (UUO) surgery for renal fibrosis indication and were treated with 50 and 100 mg/kg PCA for 14 days. Results The IC50 of PCA was appropriately 13.75 +/- 1.91 mu M in NRK-52E cells, and no significant difference at concentrations less than 5 mu M. PCA ameliorated TGF-beta 1-induced EMT, such as enhanced E-cadherin and decreased vimentin. Fibrotic markers collagen IV and alpha-smooth muscle actin (alpha-SMA) increased in TGF-beta 1-induced NRK-52E. Moreover, PCA reduced TGF-beta 1-induced migration in the wound-healing assay. Analysis of rat kidneys indicated that PCA reduced UUO-induced hydronephrosis (control: 15.11 +/- 1.00%; UUO: 39.89 +/- 1.91%; UUO + PCA50: 18.37 +/- 1.61%; UUO + PCA100: 17.67 +/- 1.39%). Protein level demonstrated that PCA not only decreased vimentin expression and enhanced E-cadherin expression, but inhibited UUO-induced collagen IV and alpha-SMA upregulation, indicating that it could mitigate EMT in a rat model of UUO-induced renal fibrosis. Discussion and conclusions This study suggested that PCA decreases TGF-beta 1-induced fibrosis and EMT in vitro and in vivo. These findings demonstrate pharmacological effects of PCA and might be a potential strategy for the prevention of organ fibrosis in clinics.

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