Inhibitory effects of curcumin on RPE–choroid production of angiogenic and inflammatory molecules.

<p>Curcumine significantly suppressed RPE–choroid protein levels of VEGF (<b>A: </b><i>n</i> = 6. *<i>P</i><0.01), TNF<i>-</i>α (<b>B: </b><i>n</i> = 6. **<i>P</i><0.05), MCP-1 (<b>C: </b><i>n</i> = 6. ***<i>P</i><0.05), and ICAM-1 (<b>D: </b><i>n</i> = 6. ****<i>P</i><0.05) on day 3. (E) Double immunostaining of F4/80 and VEGF on cryo-sections on day 3. High levels of VEGF were expressed in F4/80-positive macrophages at the photocoagulated sites. VEGF localized mainly in infiltrating macrophages at the laser injury sites. Curcumin treatment apparently decreased VEGF immunoreactivity compared to vehicle treatment. Scale bar = 100 µm.</p

Suppression of NF-κB and HIF−1α by curcumin treatment.

<p>(A) Representative Western blot showing NF- κB protein in the nuclear extract in samples from vehicle- and curcumin-treated mice 6 hours after laser injury. GAPDH was used as a loading control. (B) Semiquantitative analysis of the intensities of NF- κ B bands in nuclear extracts from vehicle- and curcumin-treated mice. The mean for NF- κ B in RPE–choroid complex of untreated mice was set at 100% (<i>n</i> = 5, *<i>P</i><0.05). (C) Representative Western blot showing HIF−1α protein expression in samples from vehicle- and curcumin-treated mice on day 3 after photocoagulation. GAPDH was used as a loading control. (D) Semiquantitative analysis of the intensities of HIF−1α bands from vehicle- and curcumin-treated mice. The mean for HIF−1α in RPE–choroid complex of untreated mice was set at 100% (<i>n</i> = 5, **<i>P</i><0.05).</p