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Curcumin targets p53-fibrinolytic system in TGF-β1 mediated alveolar epithelial mesenchymal transition in alveolar epithelial cells.

AIMS
We aim to investigate the interaction of curcumin with p53-fibrinolytic system, smad dependent and independent pathways underlying their prime role during lung injury and fibrosis.


BACKGROUND
Curcumin an active component of Curcuma longa plant substantially modulates respiratory conditions. TGFβ1 plays a central role in lung remodeling by balancing extracellular matrix (ECM) production and degradation which is a hallmark for alveolar EMT. However, it is not known yet the crosstalk of curcumin with TGF- β1 mediated p53- Fibrinolytic system regulating alveolar EMT leading to IPF. In the present study, the potential molecular mechanism of curcumin in TGF-β1 mediated p53-fibrinolytic system in basal alveolar epithelial cells was explored.


OBJECTIVES
To understand the potential molecular mechanism of curcumin in TGF-β1 mediated p53-fibrinolytic system in basal alveolar epithelial cells.


METHODS
Basal alveolar epithelial cells were treated with TGF- β1 to induce alveolar EMT and after 24 hrs curcumin were administered to study its anti-fibrotic effects. Molecular techniques like immuno blot, RT-PCR and immunofluorescence were performed to assess the anti-fibrotic role of curcumin on EMT markers, IL-17A, p53-smad interaction to investigate the anti-fibrotic role of curcumin.


RESULTS
The results indicated that TGF-β1-induced EMT in A549 cells exhibited altered expression of the IL-17A, p53- fibrinolytic markers and EMT markers at the mRNA and protein level. Intervention with curcumin attenuated alveolar EMT and inactivated TGF-β1 induced Smad/non Smad signaling pathways via blocking p53-fibrinolytic system.


CONCLUSIONS
This study provides the first evidence of the dynamic response of curcumin on TGF-β1 mediated p53- fibrinolytic system during alveolar injury in vitro.