Abstract
We investigated the effects of rapamycin (RAPA) and chloroquine (CQ) in supporting growth performance and the intestinal mucosal barrier in response to deoxynivalenol (DON) in piglets. A total of 32 healthy weaned piglets (bodyweight 7.10 ± 0.58 kg) were divided into four groups and treated daily with RAPA (1 mg/kg BW), CQ (10 mg/kg BW), or a control volume of normal saline (two groups) until the end of the experiment. After feeding a basal diet for seven days, three groups were then switched to mildewed feed containing 1 mg kg/DON for a further seven days. In contrast to the control group, DON-treated piglets showed decreased average daily gain (ADG) and daily feed intake (ADFI), as well as negatively affected intestinal morphology as indicated by villus height, crypt depth, and tight junction protein expression. A group treated with RAPA and DON showed increased intestinal autophagy, aggravated inflammatory responses, and damage to the intestinal mucosa and permeability, leading to reduced growth performance. Meanwhile, a group treated with CQ and DON showed indices comparable to the non-DON control group, with alleviated inflammatory cytokines and healthy intestinal morphology and structure. They also showed better growth performance compared to DON treatment alone. These findings have important implications for mediating autophagy against DON in vivo, as well as the potential for CQ in improving growth performance and maintaining intestinal barrier integrity in weanling piglets.
Highlights
Vomitoxin, known as deoxynivalenol (DON) [1], is one of the several mycotoxins produced by various Fusarium species that frequently grow on corn, wheat, oats, barley, rice, and other grains in the field or during storage
Administered RAPA led to poorer growth performance, further reducing the average daily gain (ADG) and average daily feed intake (ADFI) and gain: feed ratio relative to the DON group
The group receiving DON and RAPA exhibited a higher ratio of LC3II/LC3I protein and a lower level of p62 relative to the control group, while CQ treatment increased the ratio of LC3II/LC3I and expression level of p62 (Figure 1)
Summary
Known as deoxynivalenol (DON) [1], is one of the several mycotoxins produced by various Fusarium species that frequently grow on corn, wheat, oats, barley, rice, and other grains in the field or during storage It is widely found in food and animal feed, which is harmful to human health and animal husbandry development. DON shows cytotoxic, genotoxic, and visible antiproliferative effects in intestinal cells, affecting cell cycle distribution, inducing apoptosis, and inhibiting the synthesis of biomacromolecules [2,3,4]. Autophagy is a catabolic process aimed at recycling cellular components and damaged organelles in response to diverse conditions of stress, such as nutrient deprivation, viral infection, and genotoxic stress It is upregulated by Oxidative Medicine and Cellular Longevity cellular stressors to enhance cell survival [12, 13]. The knockout of the ATG5 gene led to autophagy deficiency and increased apoptosis via the generation of reactive oxygen species, suggesting that intestinal cell autophagy is essential in protecting against DON [14, 15]
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