Trans-anethole Ameliorates Intestinal Injury Through Activation of Nrf2 Signaling Pathway in Subclinical Necrotic Enteritis-Induced Broilers

Abstract

This study was conducted to investigate the alleviative effects of trans-anethole (TA) on intestinal oxidative stress by enhancing the activities of intestinal antioxidant enzymes and activating the Nrf2 signaling pathway in subclinical necrotic enteritis (NE) infected broilers. A total of 192 1-day-old male Arbor Acres broilers were randomly allocated into three treatment groups: (1) control (CON); (2) subclinical NE challenge (NE); (3) NE challenge + 600 mg/kg TA (NE+TA600). Subclinical NE was induced by oral administration of live coccidiosis vaccine containing 2 × 104 oocysts at 10 days of age and 2 ml of Clostridium perfringens type A solution (3 × 108 CFU/ml) daily from days 14 to 19. The results showed that NE infection led to a severe decline (p < 0.05) in the final body weight (BW) and average daily gain (ADG), but an increase (p < 0.05) in feed/gain (F/G) of broilers at day 10–21 and day 1–21 compared with the control group. TA administration improved (p < 0.05) the growth performance of NE birds. The intestinal villus height (VH) and villus height/crypt depth (VH/CD) were reduced (p < 0.05) by NE challenge as compared with those of the control group, which was elevated by TA administration. Subclinical NE infection decreased (p < 0.05) serum activities of total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), and jejunal and ileal glutathione peroxidase (GSH-PX), and T-SOD activity as well as T-AOC in the jejunum, while TA interventions positively elevated that (p < 0.05). Administration of TA protected the intestine against oxidative stress through up-regulation of intestinal nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway as compared with the NE group (p < 0.05). In addition, dietary inclusion of TA elevated (p < 0.05) mRNA abundance of c-mesenchymal-epithelial transition factor (c-Met), jejunal epidermal growth factor receptor (EGFR), and transforming growth factor-beta 1 (TGF-β1) in the jejunum and ileum of birds after subclinical NE challenge. In conclusion, 600 mg/kg of TA may be a promising tool to prevent and control subclinical NE by increasing intestinal antioxidant status in broilers.

Effects of Dietary Supplementation with Vitamin A on Antioxidant and Intestinal Barrier Function of Broilers Co-Infected with Coccidia and Clostridium perfringens

“…These results demonstrate that the combined infection of coccidia and C. perfringens caused oxidative stress. This is basically consistent with previous studies [ 7 ]. We observed that dietary supplementation with 12,000 IU/kg VA failed to alleviate the oxidative stress of NE-infected broilers.…”

“…A healthy intestine is a material mechanism for the high production of poultry [ 5 ]; while oxidative stress and inflammatory responses cause intestinal damage in poultry, an injured intestine opens the door for pathogenic microorganisms and stimulators, which will have negative effects on the growth performance and health of poultry [ 6 ]. Coccidia and C. perfringens are the main accomplices in necrotic enteritis (NE) in poultry, and NE causes the abnormal expression of antioxidant enzymes and peroxide products [ 7 ]. In addition, intestinal barrier-related proteins such as tight-junction proteins might be overexpressed in response to inflammation [ 8 , 9 ], and an excessive inflammatory response downregulates their expression and destroys the intestinal barrier [ 10 ].…”

Effect of Tannic Acid on Antioxidant Function, Immunity, and Intestinal Barrier of Broilers Co-Infected with Coccidia and Clostridium perfringens

“…Necrotic enteritis (NE) is a prevalent infectious gastrointestinal illness in broiler production, predominantly caused by Clostridium perfringen . C. perfringens is secondary to coccidia (coccidia is primary), or they may be co-infected, resulting in an inflammatory reaction of the intestinal mucosa and oxidative stress, which can cause a tremendous economic loss in the poultry industry [ 1 , 2 , 3 , 4 ]. Oxidative stress and inflammation disrupt mucosal cells and tight junction proteins, impeding the self-repair mechanisms of the intestinal barrier [ 5 , 6 ].…”