Abstract
This study was conducted to investigate the beneficial effects of bisdemethoxycurcumin (BDC) on growth performance, glutathione (GSH) redox potential, antioxidant enzyme defense, and gene expression in lipopolysaccharide (LPS)-challenged broilers. A total of 320, male, 1-day-old broilers were randomly assigned to 4 treatment groups including 8 replicates with 10 birds per cage in a 2 × 2 factorial arrangement: BDC supplementation (a basal diet with 0 or 150 mg/kg BDC) and LPS challenge (intraperitoneal injection of 1 mg/kg body weight saline or LPS at 16, 18, and 20 d of age). Results showed that dietary BDC supplementation prevented the LPS-induced decrease in ADG of broilers (P < 0.05). Compared to the saline-challenged group, LPS-challenged broilers showed higher jejunal and ileal malondialdehyde (MDA), protein carbonyl (PC), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) contents (P < 0.05). Dietary BDC supplementation alleviated LPS-induced increases in jejunal 8-OHdG, ileal MDA, and PC contents (P < 0.05). LPS challenge impaired the small intestinal antioxidant system, as evident by the decreases of GSH and total thiol contents, as well as superoxide dismutase (SOD), glutathione peroxidase, glutathione reductase (GR), and glutathione S-transferase (GST) activities. On the other hand, LPS challenge also increased GSH redox potential and oxidized glutathione (GSSG) contents (P < 0.05). Dietary BDC supplementation increased jejunal and ileal GSH contents, SOD activities, jejunal GR activity, and ileal GST activity, while it decreased jejunal and ileal redox potential, and jejunal GSSG contents (P < 0.05). Dietary BDC supplementation significantly alleviated the downregulation of mRNA expression levels of jejunal and ileal copper and zinc superoxide dismutase, catalytic subunit of γ-glutamylcysteine ligase, nuclear factor erythroid-2-related factor 2, heme oxygenase 1, NAD(P)H quinone oxidoreductase 1, and jejunal catalase and GR induced by LPS challenge (P < 0.05). In conclusion, BDC demonstrated favorable protection against LPS-induced small intestinal oxidative damages, as indicated by the improved growth performance, decreased GSH redox potential, enhanced antioxidant enzyme activities, and upregulated antioxidant-related gene expression.