Effects Of Fusarium Toxins On Growth Performance, Intestinal Damages And Pro-inflammatory Cytokines In Post-weaning Gilts

The aims of the present study were to investigate effects of Fusarium toxins on growth performance, activities of intestinal disaccharidase, oxidative stress, and distribution and mRNA expression levels of intestinal pro-inflammatory cytokines in post-weaning gilts. There were two phases in the test. A total of 50 healthy gilts(Duroc×Landrace×Large White) aged at 35 d with an average body weight 8.45±0.94 kg were randomly allocated into 2 treatments with 20 in the control group(Contr.) and 30 in the Fusarium toxins group(Fusarium Toxins) in the first phase. Gilts in the control group were fed a basal diet only, and the gilts in the Fusarium toxins group were fed a test diet(0.90 mg/kg ZEN, 1.43 mg/kg DON, 5.85 mg/kg FUM). Animals were fed individually in a metabolic cage for 35 d after 7 d adaptation. At the end of the first phase, 10 gilts randomly selected from each group were slaughtered and sampled simultaneously. Results showed Fusarium toxins significantly decreased(P<0.05) lactase activities of the duodenum and jejunum, sucrose activities of the jejunum and ileum, lactase activities and sucrose activities of the colon, Catalase(CAT) activities of the jejunum and ileum, total superoxide dismutase(T-SOD) and Glutathione peroxidase(GSH-Px) activities of the duodenum, ileum and colon. However, malondialdehyde(MDA) content of the jejunum and ileum, the IL-1β mRNA expression levels of duodenum, the IL-6 mRNA expression levels of duodenum and jejunum and the IL-1β and IL-6 mRNA expression levels of colon of the Fusarium toxins group were significantly higher(P<0.05) than that of the control. The mRNA expression levels of pro-inflammatory factors have a positive correlation between small intestine and colon. Because of the Fusarium toxins, the positive staining of the small intestine pro-inflammatory cytokine of IL-1β and IL-6 was from dispersed in the lamina propria cells to villous lymphocytes cytoplasmic concentration. But the IL-1β and IL-6 positive point of the colon is mainly distributed in the cytoplasm of the lamina propria cells.In the second phase, a total of 30 gilts which were left from the first phase were used. The control group was still fed the basal diet only. 20 gilts from Fusarium toxins group were randomly allocated into 2 treatments. The Fusarium toxins group was still fed the test diet and the recovery gilts(Recovery) fed the basal diet replaced the test diet. The second phase lasted for 21 d. Then all gilts were slaughtered and sampled. Results showed that Fusarium toxins significantly decreased(P<0.05) small intestinal disaccharidase activities, T-SOD and GSH-Px activities of the duodenum and disaccharidase activities of jejunum and ileum. Small intestinal MDA content of the Fusarium toxins group were higher than that of the control(P<0.05). Compared with the Fusarium toxins group, gilts of the recovery group had significantly increase in sucrose activities of duodenum, sucrose and maltase activities of jejunum and ileum, T-SOD and GSH-Px activities of the duodenum, CAT and T-SOD activities of jejunum and CAT and GSH-Px activities of ileum but small intestinal MDA content decreased significantly(P<0.05).Results showed that the average daily feed intake(ADFI) and average daily gain(ADG) of the Fusarium toxins group had significantly decreased(P<0.05) in contrast to the control, but feed to gain ratio(F/G) increased significantly(P<0.05). Compared with the Fusarium toxins group, ADG and F/G of recovery group was significantly recovered(P<0.05).It is suggested that Fusarium toxins exerted a deleterious effect on intestinal damages of gilts by the way of oxidative stress and the stimulated defensive mechanisms of intestinal in the present study, which have a negative impact on feed intake and production performance of gilts eventually. The growth performance of gilts tended to improve after stopping supply of the Fusarium toxins contaminated diet in 21 d, which shows that intestinal immunity can improve the growth performance by autoimmune repair.