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. 2018 Oct 31;9:1242. doi: 10.3389/fphar.2018.01242

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Copyright © 2018 Saito, Melo, Martinez, Fattori, Cezar, Pinto, Bussmann, Vignoli, Georgetti, Baracat, Verri and Casagrande.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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RvD1 inhibits UVB irradiation-induced oxidative stress, mRNA expression of oxidative stress-related genes and antioxidant depletion. Lipid peroxidation (A) was determined by t-butyl lipid hydroperoxides (LOOH)-initiated chemiluminescence (QL) at 4 h, superoxide anion production (B) was determined by nitroblue tetrazolium (NBT) reduction assay at 2h; gp91^phox, Nrf2 (D), Nqo-1 (E), and HO-1 (F) mRNA expression (C) were determined by quantitative polymerase chain reaction (qPCR) at 4 h after the end of irradiation; GSH levels (G) and CAT activity (H) were determined at 12 h and 2h after the end of irradiation, respectively. Bars represent means ± SEM of 5 mice per group per experiment and are representative of two separate experiments. Statistical analysis was performed by one-way ANOVA followed by Tukey's test. [*p < 0.05 compared to the non-radiated control group; ^#p < 0.05 compared to the radiated control group (vehicle)].