Inflammatory reduction via (1) Inhibition of NF-κB transcription factor and reducing the production of TNF-α, IL-1, and interferon-γ (2) Scavenging reactive oxygen species (3) Modulating production of antioxidant enzymes
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Scleroderma
Antifibrotic effect via suppressing TGF-β
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Vitiligo vulgaris
Protection against disease progression via (1) An increase in MAPK/ERK phosphorylation and inhibition of apoptosis (2) An increase in total antioxidant capacity and a decrease in intracellular reactive oxygen species generation (3) Improving mitochondrial activity
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Wound healing
Enhancing effective wound healing in three stages (a) Inflammation (see above) (b) Proliferation (1) Enhancing fibroblast migration, granulation tissue formation, collagen deposition, and re-epithelialization (2) Apoptosis in the early stage of wound healing resulting in removal of nondesirable inflammatory cells from the wound site (c) Remodeling (1) Enhancing wound closure via the production of TGF-β1 and fibronectin resulting in increased migration and proliferation of fibroblasts
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Aging
Delay the aging process via induction of Keap1-Nrf2-EpRE and phosphatidylinositol 3-kinase/Akt pathways
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Carcinogenesis
Anticarcinogenic activity in different stages of cancer (a) Transformation of normal cells into tumor cells: curcumin inhibits NF-κB and its target genes like COX-2 and cyclin D1 and induces apoptosis via activation of caspase-3, caspase-8, and Fas receptor (b) Tumor growth and progression: curcumin inhibits mTOR signaling resulting in blocking of tumor progression (c) Tumor promotion: curcumin inhibits 12-o-tetradecanoylphorbol- (TPA-) induced tumor promotion and TPA-induced tumor markers via modulation of transmembrane signal transduction via protein kinase
