Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Tanshinone IIA suppresses fibrosis induced by high glucose conditions in HK-2 cells via inhibition of extracellular matrix deposition, reduction of oxidative stress, and inhibition of epithelial to mesenchymal transition

Xi Zhao¹, Yao-Guang Wang¹ , Xi-kai Yang², Man Li³, Shi-Jie Liu², Tong-Yan Zhang⁴, Yi-Qi Wang¹

¹Nephropathy Department, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300112; ²Tianjin University of Traditional Chinese Medicine, Tianjin 301617; ³Tianjin Beichen District Chinese Medicine Hospital, Tianjin 300000; ⁴Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin 300150, PR China.

For correspondence:- Yao-Guang Wang Email: yaoguangwa@163.com Tel:+862227986573

Accepted: 24 January 2020 Published: 29 April 2020

Citation: Zhao X, Wang Y, Yang X, Li M, Liu S, Zhang T, et al. Tanshinone IIA suppresses fibrosis induced by high glucose conditions in HK-2 cells via inhibition of extracellular matrix deposition, reduction of oxidative stress, and inhibition of epithelial to mesenchymal transition. Trop J Pharm Res 2020; 19(4):739-744 doi: 10.4314/tjpr.v19i4.9

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the anti-fibrotic effects of tanshinone IIA (TS) on renal tubular epithelial cells (HK-2 cells) under high glucose conditions and their related molecular mechanism(s) of action.

Methods: After treatment with TS (6 μg/mL) for 24 h, the morphology of HK-2 cells stimulated by high glucose was observed under the microscope. Additionally, potential mechanisms related to the anti-fibrosis effects of TS were evaluated using western blotting assay and quantitative real time PCR (qRT-PCR), including transforming growth factor (TGF) β1, α-smooth muscle actin (α-SMA), heme oxygenase 1 (HO-1), laminin (LN), fibronectin (FN), and E-cadherin (E-cad).

Results: A high-glucose culture environment induced fibrosis of HK-2 cells, as indicated by changes in cell morphology. The anti-fibrotic effects of TS were mainly associated with a decrease in the expression levels of TGF-β1, α-SMA and LN, while the expression of E-cad increased. These results also revealed that TS increased the expressions of HO-1.

Conclusion: The findings suggest that TS suppresses fibrosis caused by high glucose in HK-2 cells by inhibiting extracellular matrix deposition and epithelial-mesenchymal transition and by reducing oxidative stress. Further investigations are needed to evaluate the clinical application of this compound in diabetic nephropathy.

Keywords: Tanshinone IIA, Diabetic nephropathy, HK-2 cells, Fibrosis