BACKGROUND: Resveratrol has been shown to prevent high ambient temperature (HT)-induced spleen dysplasia, but the mechanisms of action are not clear. This study aims to examine the hypothesis that HT-induced spleen dysplasia may be associated with HT-induced oxidative stress and apoptosis, and resveratrol may activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, thus reducing oxidative stress and apoptosis. RESULTS: Results showed that HT caused spleen dysplasia in broilers, reflecting the lower relative weight of the spleen (P < 0.05). Compared with birds in a normal ambient temperature group, birds in the HT group exhibited higher (P < 0.05) malondialdehyde (MDA), protein carbonyl (PC), 8-hydroxydeoxyguanosine (8-OHdG) and Bcl-2 associated X protein (Bax) content, higher Bax, caspase-3 and caspase-9 mRNA levels, and caspase-3 and caspase-9 activity, and a higher Bax/B-cell lympoma/leukemia-2 (Bcl-2) ratio, but they exhibited lower (P < 0.05) glutathione (GSH) and Bcl-2 content, and lower Nrf2, glutathione peroxidase (Gpx), MnSOD, heme oxygenase 1, glutathione reductase (GR) and Bcl-2 mRNA levels, and lower total antioxidant capacity (T-AOC), T-SOD and catalase and maganese superoixide dismutase (CAT) activity, indicating HT-induced oxidative stress and apoptosis. Compared with birds in the HT group, birds in the HT + Res group exhibited higher (P < 0.05) GSH and Bcl-2 content, higher Nrf2, CAT, MnSOD, GR and Bcl-2 mRNA levels, and higher T-AOC, T-SOD and CAT activity, but lower (P < 0.05) MDA content, and Bax and caspase-3 mRNA levels, lower caspase-3 and caspase-9 activities, and Bax/Bcl-2 ratio, indicating that resveratrol activated the Nrf2 signaling pathway and decreased apoptosis in the spleen. CONCLUSION: Resveratrol was effective in ameliorating HT-induced spleen dysplasia in broilers through the activation of the Nrf2 signaling pathway, thereby decreasing apoptosis, suggesting that resveratrol may offer a potential nutritional strategy to protect against some HT-induced detriments.
BACKGROUND:Resveratrol has been shown to prevent high ambient temperature (HT)-induced spleen dysplasia, but the mechanisms of action are not clear. This study aims to examine the hypothesis that HT-induced spleen dysplasia may be associated with HT-induced oxidative stress and apoptosis, and resveratrol may activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, thus reducing oxidative stress and apoptosis. RESULTS: Results showed that HT caused spleen dysplasia in broilers, reflecting the lower relative weight of the spleen (P < 0.05). Compared with birds in a normal ambient temperature group, birds in the HT group exhibited higher (P < 0.05) malondialdehyde (MDA), protein carbonyl (PC), 8-hydroxydeoxyguanosine (8-OHdG) and Bcl-2 associated X protein (Bax) content, higher Bax, caspase-3 and caspase-9 mRNA levels, and caspase-3 and caspase-9 activity, and a higher Bax/B-cell lympoma/leukemia-2 (Bcl-2) ratio, but they exhibited lower (P < 0.05) glutathione (GSH) and Bcl-2 content, and lower Nrf2, glutathione peroxidase (Gpx), MnSOD, heme oxygenase 1, glutathione reductase (GR) and Bcl-2 mRNA levels, and lower total antioxidant capacity (T-AOC), T-SOD and catalase and maganese superoixide dismutase (CAT) activity, indicating HT-induced oxidative stress and apoptosis. Compared with birds in the HT group, birds in the HT + Res group exhibited higher (P < 0.05) GSH and Bcl-2 content, higher Nrf2, CAT, MnSOD, GR and Bcl-2 mRNA levels, and higher T-AOC, T-SOD and CAT activity, but lower (P < 0.05) MDA content, and Bax and caspase-3 mRNA levels, lower caspase-3 and caspase-9 activities, and Bax/Bcl-2 ratio, indicating that resveratrol activated the Nrf2 signaling pathway and decreased apoptosis in the spleen. CONCLUSION:Resveratrol was effective in ameliorating HT-induced spleen dysplasia in broilers through the activation of the Nrf2 signaling pathway, thereby decreasing apoptosis, suggesting that resveratrol may offer a potential nutritional strategy to protect against some HT-induced detriments.