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. 2026 Aug 24;17:1691999. doi: 10.3389/fphar.2026.1691999

FIGURE 5.

Infographic illustrating the mechanisms by which various curcumin nanomaterials mitigate inflammation, fibrosis, and cellular injury in liver and airway tissues, using labeled molecular pathways, cell types, and annotated signaling cascades.

Curcumin (CUR) nanoparticles involved in the figures include 3-carboxypropyl-triphenylphosphonium bromide-poly(ethylene glycol)-poly(ε-caprolactone) (CTPP–PEG–PCL) micelles, CUR-silver nanoparticles (AgNPs), sophorolipid-coated CUR nanoparticles, GCNp-CUR NPs, CEHPNPs, CUR-loaded large porous microparticles (CURLPMPs), manganese–CUR metal–organic frameworks (MOFs), and liposome-encapsulated curcumin. CUR nanoparticles alleviate liver fibrosis by reducing oxidative stress [reactive oxygen species (ROS), H2O2, ferritin; activating superoxide dismutase (SOD)], suppressing inflammation (TNF-α, IL-1β, IL-6, and NF-κB P65; upregulating IL-10), inhibiting fibrosis [PDGF/transforming growth factor β1 (TGF-β1), collagen I, α-smooth muscle actin (α-SMA), and tissue inhibitor of metalloproteinase (TIMP)-1], modulating MAPK/p-extracellular-regulated protein kinase (ERK)/p-JAK pathways, and improving non-alcoholic fatty liver disease (NAFLD) markers (TG and TC), leading to reduced necrosis and myofibroblast activation.