Journal of biosciences | |
Andrographolide suppresses epithelial mesenchymal transition by inhibition of MAPK signalling pathway in lens epithelial cells | |
Forum Kayastha1  Abhay Vasavada11  Hardik Madhu1  Kaid Johar1  Darshini Ganatra1  Devarshi Gajjar2  Anshul Arora1  | |
[1] Iladevi Cataract and IOL Research Centre, Gurukul road, Memnagar, Ahmedabad 380 052, India$$;Department of Microbiology and Biotechnology Centre, Faculty of Science, MS University of Baroda, Vadodara 390 002, India$$ | |
关键词: Andrographolide; bFGF; epithelial mesenchymal transition; lens epithelial cells; MAPK signalling; TGF-ð›½; | |
DOI : | |
来源: Indian Academy of Sciences | |
【 摘 要 】
Epithelial mesenchymal transition (EMT) of lens epithelial cells (LECs) may contribute to the development of posterior capsular opacification (PCO), which leads to visual impairment. Andrographolide has been shown to have therapeutic potential against various cancers. However, its effect on human LECs is still unknown. The purpose of this study is to evaluate the effect of andrographolide on EMT induced by growth factors in the fetal human lens epithelial cell line (FHL 124). Initially the LECs were treated with growth factors (TGF-ð›½2 and bFGF) to induce EMT. Subsequently these EMT-induced cells were treated with andrographolide at 100 and 500 nM concentrations for 24 h. Our results showed that FHL 124 cells treated with growth factors had a significant decrease in protein and m-RNA levels of epithelial markers pax6 and E-Cadherin. After administering andrographolide, these levels significantly increased. It was noticed that EMT markers ð›¼-SMA, fibronectin and collagen IV significantly decreased after treatment with andrographolide when compared to the other group. Treatment with andrographolide significantly inhibited phosphorylation of ERK and JNK. Cell cycle analysis showed that andrographolide did not arrest cells at G0/G1 or G2/M at tested concentrations. Our findings suggest that andrographolide helps sustain epithelial characteristics by modulating EMT markers and inhibiting the mitogen-activated protein kinase (MAPK) signalling pathway in LECs. Hence it can prove to be useful in curbing EMT-mediated PCO.
【 授权许可】
Unknown
【 预 览 】
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