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Article

Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells

  • Authors:
    • Dandan Li
    • Tingbao Zhao
    • Jianzhong Meng
    • Ying Jing
    • Fengyu Jia
    • Ping He
  • View Affiliations / Copyright

    Affiliations: Department of Spinal Cord Repair, General Hospital of Jinan Military Region, PLA, Jinan, Shandong 250031, P.R. China, Department of Blood Purification, General Hospital of Jinan Military Region, PLA, Jinan, Shandong 250031, P.R. China
  • Pages: 8148-8154
    |
    Published online on: October 15, 2015
       https://doi.org/10.3892/mmr.2015.4445
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Abstract

Diabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed ‘epithelial‑mesenchymal transition’ (EMT) results in fibrosis of renal tubular epithelial cells, and is key in DN. As an antioxidant, procyanidin B2 can inhibit cardiac fibrosis; however, whether it has an effect on the inhibition of renal fibrosis remains to be elucidated. The present study demonstrated that high glucose levels were able to activate EMT‑associated changes, including the loss of E‑cadherin and increase in α‑smooth muscle actin (α‑SMA), as determined by western blotting and immunofluorescence. Pre‑treatment with procyanidin B2 reversed the high glucose‑induced morphological changes, upregulated the expression of E‑cadherin and downregulated the expression levels of vimentin and α‑SMA. Furthermore, procyanidin B2 decreased the phosphorylation of small mothers against decapentaplegic (Smad)2, Smad3 and P38, and upregulated the expression of phosphorylated‑Smad7. In conclusion, the results of the present study suggested that procyanidin B2 inhibited high glucose‑induced EMT through the inhibition of transforming growth factor‑β/Smad and mitogen‑activated protein kinase/P38 signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Li D, Zhao T, Meng J, Jing Y, Jia F and He P: Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells. Mol Med Rep 12: 8148-8154, 2015.
APA
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., & He, P. (2015). Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells. Molecular Medicine Reports, 12, 8148-8154. https://doi.org/10.3892/mmr.2015.4445
MLA
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., He, P."Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells". Molecular Medicine Reports 12.6 (2015): 8148-8154.
Chicago
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., He, P."Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells". Molecular Medicine Reports 12, no. 6 (2015): 8148-8154. https://doi.org/10.3892/mmr.2015.4445
Copy and paste a formatted citation
x
Spandidos Publications style
Li D, Zhao T, Meng J, Jing Y, Jia F and He P: Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells. Mol Med Rep 12: 8148-8154, 2015.
APA
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., & He, P. (2015). Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells. Molecular Medicine Reports, 12, 8148-8154. https://doi.org/10.3892/mmr.2015.4445
MLA
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., He, P."Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells". Molecular Medicine Reports 12.6 (2015): 8148-8154.
Chicago
Li, D., Zhao, T., Meng, J., Jing, Y., Jia, F., He, P."Procyanidin B2 inhibits high glucose‑induced epithelial‑mesenchymal transition in HK‑2 human renal proximal tubular epithelial cells". Molecular Medicine Reports 12, no. 6 (2015): 8148-8154. https://doi.org/10.3892/mmr.2015.4445
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