PAI-1 influences and curcumin destabilizes MMP-2, MMP-9 and basement membrane proteins during lung injury and fibrosis.
AI Summary
Key Findings
Abstract
One of the characteristic feature of idiopathic pulmonary fibrosis is an imbalanced fibrinolytic system. Plasminogen activator inhibitor-1 (PAI-1), an essential serine protease in the fibrinolytic system, has an anti-fibrotic tendency in some organs and a pro-fibrotic nature in others. Curcumin is reported to regulate the fibrinolytic system. In this study, we sought to determine how curcumin affected alterations in tissue remodelling mediated by PAI-1 in lung fibrosis. For in vitro studies, NIH3T3 fibroblasts were either exposed to TGF-βor overexpressed with PAI-1, and/or treated with curcumin. For in vivo studies, C57BL/6 mice were either instilled with bleomycin, overexpressed with PAI-1, and/or intervened with curcumin. Protein and gene expression studies were performed by western blotting and RT-PCR techniques, respectively. Curcumin intervention, in vitro and in vivo, could inhibit the the expression of collagen, fibronectin, MMP-2, and MMP-9, which was otherwise elevated by TGF-βor bleomycin. In conclusion, curcumin reduces pulmonary fibrosis by suppressing excessive basement membrane protein deposition and, likely, preventing the thickening of the alveolar septum.
Affiliation
Fathimath Muneesa Moideen
External References
- PubMed ID:
- 39549545
Comments
Sign in or create a free account to join the conversation.
Sign in to commentBe the first to comment.