Dietary chitosan oligosaccharides alleviate heat stress-induced intestinal oxidative stress and inflammatory response...

The purpose of this study was to evaluate the effects of chitosan oligosaccharides (COS) on intestinal permeability, morphology, antioxidant status, and inflammatory response in heat-stressed broilers. A total of 108 thirty-five-day-old Chinese yellow-feather broilers (body weight 470.31 ± 13.15 g) were randomly allocated to 3 dietary treatments as follows: CON group, basal diet and raised under normal temperature (24°C); HS group, basal diet and raised under cycle heat stress (34°C from 10:00-18:00 and 24°C for the rest time); HSC group, basal diet with 200 mg/kg COS supplementation and raised under cycle heat stress. Each treatment had 6 replication pens and 6 broilers per pen. Compared with the CON group, heat stress decreased (P < 0.05) the relative weight of duodenum and jejunum; the relative length and villus height (VH) of duodenum, jejunum, and ileum; the ileum VH to crypt depth ratio; duodenum mucosal catalase (CAT) activity; and jejunum mucosal glutathione peroxidase (GSH-Px) and CAT activity, whereas it increased (P < 0.05) serum diamine oxidase (DAO) activity and D-lactate acid (D-LA) content, duodenum and jejunum mucosal malondialdehyde (MDA) and interleukin-1β (IL-1β) content, and ileum mucosal tumor necrosis factor-α content. Compared to the HS group, dietary COS supplementation increased (P < 0.05) the relative length of duodenum, jejunum, and ileum; the VH of jejunum and ileum; and duodenum and jejunum mucosal GSH-Px activity, whereas it decreased (P < 0.05) serum DAO activity and D-LA concentration and duodenum and jejunum mucosal MDA and IL-1β content. These results suggested that dietary COS supplementation had beneficial effects on intestinal morphology by increasing jejunum and ileum VH; permeability by decreasing serum DAO activity and D-LA content; antioxidant capacity by decreasing duodenum and jejunum mucosal MDA content and by increasing duodenum and jejunum GSH-Px activity; and inflammatory response by decreasing duodenum and jejunum mucosal IL-1β content.