Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 85, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2020.106676
Keywords
IL-17A; AMPK alpha; COX-2; Lung injury; Curcumin; NF kappa B
Categories
Funding
- Department of Biotechnology (DBT) Grant [BT/PR25198/MED/30/1896/2017]
- Yenepoya (Deemed to be University)
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Acute lung injury (ALI) remains to be the major cause of mortality. Bleomycin (BLM) injury activates the proinflammatory cytokine Interleukin L-17A which regulates the expression of COX-2 and inhibits P-AMPK alpha in BLM/IL-17A exposed mice upon activation of NF kappa B and other inflammatory molecules the actual mechanism behind which remains unclear. The current investigation was carried out to assess the role of IL-17A with COX-2 and P-AMPK alpha and to highlight the important contribution of adjunctive use of curcumin as a promising preventive strategy for the BLM-induced ALI. Immunofluorescence analysis reveals that the natural spice curcumin blocks the expressions of COX-2, NF-kappa B-p65, fibronectin (FBN), and expresses P-AMPK alpha in vivo. Curcumin could also suppress the expressions of NF-kappa B-p105 in BLM/IL-17A exposed mice. mRNA expressions showed reduced expressions of PDGFA, PDGFB, CTGF, IGF1, NF kappa B1, NF kappa B2, MMP-3, MMP-9, and MMP-14 on curcumin treatment. Our study implicates a critical role of AMPK alpha/COX-2 in the emergence of pulmonary fibrosis via exerting the potential role of curcumin as an adjuvant anti-inflammatory therapeutic for treating lung injury.
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