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

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.