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Andrographolide suppresses epithelial mesenchymal transition by inhibition of MAPK signalling pathway in lens
Forum Kayastha1, Kaid Johar, Devarshi Gajjar
1Iladevi Cataract and IOL Research Centre, Gurukul road, Memnagar, Ahmedabad 380 052, India.
Abstract:
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-beta 2 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 alpha-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.
Insights
Andrographolide may prevent posterior capsular opacification (PCO) by inhibiting epithelial mesenchymal transition (EMT) in lens epithelial cells (LECs). This natural compound helps maintain epithelial cell characteristics, offering potential therapeutic benefits for vision impairment.
Area of Science:
- Ophthalmology
- Cell Biology
- Pharmacology
Background:
- Epithelial mesenchymal transition (EMT) in lens epithelial cells (LECs) is implicated in posterior capsular opacification (PCO), a cause of visual impairment.
- Andrographolide, known for anti-cancer properties, has not been studied for its effects on human LECs or EMT.
Purpose of the Study:
- To investigate the effect of andrographolide on growth factor-induced EMT in a human fetal lens epithelial cell line (FHL 124).
Main Methods:
- Lens epithelial cells (LECs) were induced to undergo EMT using TGF-beta 2 and bFGF.
- Cells were subsequently treated with andrographolide (100 and 500 nM) for 24 hours.
- Analysis included epithelial and EMT marker expression, MAPK pathway activity (ERK, JNK phosphorylation), and cell cycle progression.
Main Results:
- Andrographolide treatment increased epithelial markers (Pax6, E-Cadherin) and decreased EMT markers (alpha-SMA, fibronectin, collagen IV) in FHL 124 cells.
- It significantly inhibited ERK and JNK phosphorylation, key components of the MAPK signaling pathway.
- Andrographolide did not induce cell cycle arrest at the tested concentrations.
Conclusions:
- Andrographolide suppresses EMT in LECs by modulating EMT markers and inhibiting the MAPK signaling pathway.
- This suggests andrographolide's potential as a therapeutic agent to prevent or treat EMT-mediated PCO and preserve vision.
