Background: Bleomycin (BLM) is known to cause DNA damage in the alveolar epithelial
cells (AECs). It is reported that BLM is involved in the up-regulation of inflammatory molecules such
as neutrophils, macrophages, chemokines and cytokines. The complex underlying mechanism for
inflammation mediated progression of lung injury is still unclear. This investigation was designed to
understand the molecular mechanisms associated with p53 mediated modulation of plasminogen activator
inhibitor-I (PAI-I) expression and its regulation by nano-curcumin formulation.
Methods: A549 cells were treated with BLM to cause the cellular damage in vitro and commercially
available nano-curcumin formulation was used as an intervention. Cytotoxic effect of nano-curcumin
was analyzed using Methyl thiazolyl tetrazolium (MTT) assay. Protein expressions were analyzed using
western blot to evaluate the p53 mediated changes in PAI-I expression.
Results: Nano-curcumin showed cytotoxicity up to 88.5 % at a concentration of 20 µg/ml after 48 h of
treatment. BLM exposure to the cells activated the phosphorylation of p53, which in turn increased PAII
expression. Nano-curcumin treatment showed a protective role against phosphorylation of p53 and
PAI-I expression, which in turn regulated the fibro-proliferative phase of injury induced by bleomycin.
Conclusion: Nano-curcumin could be used as an effective intervention to regulate the severity of lung
injury, apoptosis of AECs and fibro-proliferation during pulmonary injury.
Keywords: Bleomycin, alveolar basal epithelial cells, nano-curcumin, p53, PAI-1
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