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. 2014 Jun 16;111(26):9603–9608. doi: 10.1073/pnas.1401191111

Fig. 4.

Fig. 4.

Dietary ω-3 LCPUFAs up-regulate PPARγ signaling and attenuate laser-induced CNV in a PPARγ-dependent manner. (A) PPARγ activity as determined with an ELISA in nuclear extracts of the retina at 7 d after CNV induction in mice fed ω-6 or ω-3 LCPUFAs. Data are expressed as means ± SEM of absorbance at 450 nm (A450) (n = 6). ***P < 0.001. (B) (Upper) Lesion size as determined in choroidal flat-mount preparations at 7 d after CNV induction for mice fed ω-3 LCPUFAs, mice fed ω-6 LCPUFAs, or mice fed ω-3 LCPUFAs injected i.p. with the PPARγ inhibitor GW9662 (GW, 1 mg/kg) daily beginning immediately after photocoagulation. Data are presented as means ± SEM (n = 50–73 lesions). ‡P < 0.05, ‡‡P < 0.01. (Lower) Representative staining of CNV. (Scale bar: 50 μm.) (C) (Upper) Cross-sectional area of lesions as determined by SD-OCT for mice treated as in B. Data are presented as means ± SEM (n = 36–69 lesions). ‡‡‡P < 0.001. (Lower) Representative images. (Scale bars: 50 μm.) (D) PPARγ activity in nuclear extracts of the retina for mice treated as in B. Data are presented as means ± SEM (n = 6). ‡P < 0.05, ‡‡‡P < 0.001.