The Journal of nutrition · 2024
Alginate Oligosaccharides Enhance Gut Microbiota and Intestinal Barrier Function, Alleviating Host Damage Induced by Deoxynivalenol in Mice.
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Mi Jinqiu, Tong Yaoyi, Zhang Qiyue, Wang Qingfeng, Wang Yanwei, Wang Yue, Lin Gang, Ma Qiugang, Li Tiantian, Huang Shimeng
Аннотация
BACKGROUND: Alginate oligosaccharides (AOS) exhibits notable effects in terms of anti-inflammatory, antibacterial, and antioxidant properties. Deoxynivalenol (DON) has the potential to trigger intestinal inflammation by upregulating pro-inflammatory cytokines and apoptosis, thereby compromising the integrity of the intestinal barrier function and perturbing the balance of the gut microbiota.
OBJECTIVES: We assessed the impact of AOS on mitigating DON-induced intestinal damage and systemic inflammation in mice.
METHODS: After a 1-wk acclimatization period, the mice were divided into 4 groups. For 3 wk, the AOS and AOS + DON groups were gavaged daily with 200 μL of AOS [200 mg/kg body weight (BW)], whereas the CON and DON groups received an equivalent volume of sterile Phosphate-Buffered Saline (PBS). Subsequently, for 1 wk, the DON and AOS + DON groups received 100 μL of DON (4.8 mg/kg BW) daily, whereas the control (CON) and AOS groups continued receiving PBS.
RESULTS: After administering DON via gavage to mice, there was a significant decrease (P < 0.05) in body weights compared with the CON group. Interestingly, AOS exhibited a tendency to mitigate this weight loss in the AOS + DON group. In the feces of mice treated with both AOS and DON, the concentration of DON significantly increased (P < 0.05) compared with the DON group alone. Histological analysis revealed that DON exposure caused increased intestinal damage, including shortened villi and eroded epithelial cells, which was ameliorated by presupplementation with AOS, alleviating harm to the intestinal barrier function. In both jejunum and colon tissues, DON exposure significantly reduced (P < 0.05) the expression of tight junction proteins (claudin and occludin in the colon) and the mucin protein mucin 2, compared with the CON group. Prophylactic administration of AOS alleviated these reductions, thereby improving the expression levels of these key proteins. Additionally, AOS supplementation protected DON-exposed mice by increasing the abundance of probiotics such as Bifidobacterium, Faecalibaculum, and Romboutsia. These gut microbes are known to enhance (P < 0.05) anti-inflammatory responses and the production of short-chain fatty acids (SCFAs), including total SCFAs, acetate, and valerate, compared with the DON group.
CONCLUSIONS: This study unveils that AOS not only enhances gut microbiota and intestinal barrier function but also significantly mitigates DON-induced intestinal damage.
OBJECTIVES: We assessed the impact of AOS on mitigating DON-induced intestinal damage and systemic inflammation in mice.
METHODS: After a 1-wk acclimatization period, the mice were divided into 4 groups. For 3 wk, the AOS and AOS + DON groups were gavaged daily with 200 μL of AOS [200 mg/kg body weight (BW)], whereas the CON and DON groups received an equivalent volume of sterile Phosphate-Buffered Saline (PBS). Subsequently, for 1 wk, the DON and AOS + DON groups received 100 μL of DON (4.8 mg/kg BW) daily, whereas the control (CON) and AOS groups continued receiving PBS.
RESULTS: After administering DON via gavage to mice, there was a significant decrease (P < 0.05) in body weights compared with the CON group. Interestingly, AOS exhibited a tendency to mitigate this weight loss in the AOS + DON group. In the feces of mice treated with both AOS and DON, the concentration of DON significantly increased (P < 0.05) compared with the DON group alone. Histological analysis revealed that DON exposure caused increased intestinal damage, including shortened villi and eroded epithelial cells, which was ameliorated by presupplementation with AOS, alleviating harm to the intestinal barrier function. In both jejunum and colon tissues, DON exposure significantly reduced (P < 0.05) the expression of tight junction proteins (claudin and occludin in the colon) and the mucin protein mucin 2, compared with the CON group. Prophylactic administration of AOS alleviated these reductions, thereby improving the expression levels of these key proteins. Additionally, AOS supplementation protected DON-exposed mice by increasing the abundance of probiotics such as Bifidobacterium, Faecalibaculum, and Romboutsia. These gut microbes are known to enhance (P < 0.05) anti-inflammatory responses and the production of short-chain fatty acids (SCFAs), including total SCFAs, acetate, and valerate, compared with the DON group.
CONCLUSIONS: This study unveils that AOS not only enhances gut microbiota and intestinal barrier function but also significantly mitigates DON-induced intestinal damage.