Potential effects of curcumin on peroxisome proliferator-activated receptor-γ in vitro and in vivo

Figure 1 Possible mechanisms, primarily the inhibition of hepatic stellate cell activation by peroxisome proliferator-activated receptor-γ after modulation with curcumin. PPAR-γ: Peroxisome proliferator-activated receptor-γ; HSC: Hepatic stellate cell; TGF: Transforming growth factor; Cur: Curcumin; ECM: Extracellular matrix.

Figure 2 Liver fibrosis creation followed down-regulating of peroxisome proliferator-activated receptor-γ after liver injury. As shown, decrease in PPAR-γ expression after liver injury causes an increase in HSC DNA expression and HSC activation. This regulation also results in increased expression of α-SMA, collagen, ECM and TGF-β and induces liver fibrosis. PPAR-γ: Peroxisome proliferator-activated receptor-γ; HSC: Hepatic stellate cell; TGF: Transforming growth factor; ECM: Extracellular matrix; α-SMA: α-smooth muscle actin.

Figure 3 Mechanisms of anti-inflammatory properties of curcumin in vivo. Curcumin (Cur) down-regulates some of the factors involved in inflammation, inhibiting NF-κB activation and causing its anti-inflammatory effects. Also, Cur with increasing PPAR-γ expression directly inhibits NF-κB activation. NF-κB: Nuclear factor kappa B; TNF: Tumor necrosis factors; MCP-1: Monocyte chemoattractant protein-1; IL: Interleukins; LOX: Lipoxygenase; COX: Cyclooxygenase; iNOS: Inducible nitric oxide synthase; STAT3: Signal transducer and activator of transcription 3; PPAR-γ: Peroxisome proliferator-activated receptor-γ; XO: Xanthine oxidase.