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Allicin inhibits tubular epithelial‑myofibroblast transdifferentiation under high glucose conditions in vitro

  • Authors:
    • Hong Huang
    • Fenping Zheng
    • Xuehong Dong
    • Fang Wu
    • Tianfeng Wu
    • Hong Li

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  • Published online on: November 18, 2016     https://doi.org/10.3892/etm.2016.3913
  • Pages: 254-262
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Abstract

Previous studies have suggested that tubular epithelial-mesenchymal transition (EMT) is an important event in renal tubulointerstitial fibrosis, which is a clinical characteristic of diabetic nephropathy. The present study aimed to investigate the effect of allicin, the major biological active component of garlic, on the EMT of a human renal proximal tubular epithelial cell line (HK‑2) cultured under high glucose concentrations. HK‑2 cells were exposed for 48 h to 5.5 or 25 mmol/l D‑glucose, 25 mmol/l D‑glucose plus allicin (2.5, 5, 10 or 20 µg/ml) or 25 mmol/l D‑glucose plus 20 µmol/l PD98059, a selective inhibitor of the mitogen activated protein kinase/extracellular signal‑regulated kinase (ERK) signaling pathway. The EMT of HK‑2 cells was assessed by analyzing the protein expression of E‑cadherin, α‑smooth muscle actin (α‑SMA), vimentin and collagen I via immunocytochemistry. In addition, reverse transcription‑quantitative polymerase chain reaction and western blotting were used to detect the expression levels of transforming growth factor (TGF)‑β1 and phosphorylated (p)‑ERK1/2. Marked morphological changes were observed in HK‑2 cells cultured under high glucose conditions, and these changes were abrogated by simultaneous incubation with allicin and PD98059. The expression levels of α‑SMA, vimentin and collagen I were significantly increased in HK‑2 cells cultured under high glucose conditions, as compared with those cultured under normal glucose conditions (P<0.01). Conversely, the expression levels of E‑cadherin were significantly decreased upon stimulation with high glucose (P<0.01). Furthermore, the expression levels of TGF‑β1 and p‑ERK1/2 were significantly upregulated in HK‑2 cells cultured under high glucose conditions, as compared with those cultured under normal glucose conditions (P<0.05). Allicin partially reversed the high‑glucose‑induced increase in α‑SMA, vimentin and collagen I expression (P<0.01 at 20 µg/ml), increased the expression of E‑cadherin, and significantly downregulated the high glucose‑induced expression of TGF‑β1 and p‑ERK1/2 in a dose‑dependent manner (P<0.05). The results of the present study suggested that high glucose concentrations induced the EMT of HK‑2 cells, and that allicin was able to inhibit the EMT, potentially via regulation of the ERK1/2‑TGF‑β1 signaling pathway.
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January-2017
Volume 13 Issue 1

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Spandidos Publications style
Huang H, Zheng F, Dong X, Wu F, Wu T and Li H: Allicin inhibits tubular epithelial‑myofibroblast transdifferentiation under high glucose conditions in vitro. Exp Ther Med 13: 254-262, 2017.
APA
Huang, H., Zheng, F., Dong, X., Wu, F., Wu, T., & Li, H. (2017). Allicin inhibits tubular epithelial‑myofibroblast transdifferentiation under high glucose conditions in vitro. Experimental and Therapeutic Medicine, 13, 254-262. https://doi.org/10.3892/etm.2016.3913
MLA
Huang, H., Zheng, F., Dong, X., Wu, F., Wu, T., Li, H."Allicin inhibits tubular epithelial‑myofibroblast transdifferentiation under high glucose conditions in vitro". Experimental and Therapeutic Medicine 13.1 (2017): 254-262.
Chicago
Huang, H., Zheng, F., Dong, X., Wu, F., Wu, T., Li, H."Allicin inhibits tubular epithelial‑myofibroblast transdifferentiation under high glucose conditions in vitro". Experimental and Therapeutic Medicine 13, no. 1 (2017): 254-262. https://doi.org/10.3892/etm.2016.3913