Curcumin attenuates heat-stress-induced oxidant damage by simultaneous activation of GSH-related antioxidant enzymes and Nrf2-mediated phase II detoxifying enzyme systems in broiler chickens

The object of this study was to investigate the effect of curcumin on modulating the glutathione (GSH)-related antioxidant enzymes and antioxidant responses via NF-E2-related factor 2 (Nrf2) signaling pathway in heat-stressed broiler chickens. A total of 400 one-day-old male Arbor Acres broiler chicks was reared in an environmentally controlled room. At 21 d, broiler chicks were divided into 5 treatment groups and were fed one of 4 diets under 2 temperature conditions: 22 degrees C + a basal diet (CON treatment); 34 degrees C for 8 h (0900-1700) + a basal diet supplemented with 0, 50, 100, or 200 mg/kg curcumin (HS, CMN1, CMN2, and CMN3 treatments, respectively). The heat treatment lasted for 20 consecutive days. The results showed that heat stress significantly increased (P < 0.05) the weekly rectal temperature and average head and feet temperature. Compared to the HS treatment, feed conversion was significantly decreased (P < 0.05) in CMN1 and CMN2 treatments. CMN1 administration significantly improved (P < 0.05) the pH(24) of muscle. The abnormal changes of serum malonaldehyde and corticosterone concentrations were prevented (P < 0.05) by curcumin. Mitochondrial GSH concentration in the liver was significantly increased (P < 0.05) in CMN1 and CMN2 treatments compared with the HS treatment. The CMN1, CMN2, and CMN3 supplementations significantly increased (P < 0.05) gamma-GCL, GSH-Px, and GST activities. Curcumin significantly increased (P < 0.05) the expression of Nrf2, HO-1, and gamma-GCLc in the liver as compared to the CON diet. The expression of Cu/ZnSOD and CAT were increased (P < 0.05) by feeding CMN2, respectively, as compared to the HS treatment. It was concluded that curcumin supplementation enhanced the resistance of broilers to heat stress, as evidenced by reversing the FC, increasing the GSH content and GSH-related enzyme activities, and inducing the expression of Nrf2 and Nrf2-mediated phase II detoxifying enzyme genes.