Halofuginone prevents extracellular matrix deposition in diabetic nephropathy

2009 ◽  
Vol 379 (2) ◽  
pp. 411-416 ◽  
Author(s):  
Seiya Sato ◽  
Harukiyo Kawamura ◽  
Minoru Takemoto ◽  
Yoshiro Maezawa ◽  
Masaki Fujimoto ◽  
...  
Cell Reports ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 199-212.e5 ◽  
Author(s):  
Hirokazu Muraoka ◽  
Kazuhiro Hasegawa ◽  
Yusuke Sakamaki ◽  
Hitoshi Minakuchi ◽  
Takahisa Kawaguchi ◽  
...  

2020 ◽  
Vol 19 (4) ◽  
pp. 739-744
Author(s):  
Xi Zhao ◽  
Yao-Guang Wang ◽  
Xi-kai Yang ◽  
Man Li ◽  
Shi-Jie Liu ◽  
...  

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 antifibrosis effects of TS were evaluated using western blotting assay and quantitative real time PCR (qRTPCR), 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 resultsalso 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


2021 ◽  
Author(s):  
Hao Li ◽  
Mengna Li ◽  
Pei Liu ◽  
Kai-Yang Wang ◽  
Haoyu Fang ◽  
...  

Due to the native skin limitations and the complexity of reconstructive microsurgery, advanced biomaterials are urgently required to promote wound healing for severe skin defects caused by accidents and disasters....


2021 ◽  
Vol 19 (4) ◽  
pp. 501-507
Author(s):  
Yunhe Gu ◽  
Peiyao Guo ◽  
Guangbiao Xu

Transforming growth factor-β1 promotes excessive extracellular matrix deposition and epithelial-mesenchymal transition of tubular epithelial cells, thus stimulating the progression of renal fibrosis. Carvacrol has been shown to alleviate cardiac and liver fibrosis and attenuate renal injury. However, the role of carvacrol on renal fibrosis has not been examined. First, measurements using Cell Counting Kit-8 showed that carvacrol reduced cell viability of tubular epithelial cell line HK-2 in a dose-dependent fashion. Second, transforming growth factor-β1 induced excessive extracellular matrix deposition in HK-2 cells with enhanced collagen I, collagen IV, and fibronectin expression. However, carvacrol decreased the expression of collagen I, collagen IV in a dose-dependent manner and fibronectin to attenuate the extracellular matrix deposition in HK-2. Third, carvacrol attenuated TGF-β1-induced decrease of E-cadherin and increase of snail, vimentin, and alpha-smooth muscle actin in HK-2 cells. Transforming growth factor-β1-induced increase in PI3K and AKT phosphorylation in HK-2 were also reversed by carvacrol. Collectively, carvacrol ameliorates renal fibrosis through inhibition of transforming growth factor-β1-induced extracellular matrix deposition and epithelial-mesenchymal transition of HK-2 cells, providing potential therapy for the treatment of renal fibrosis.


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