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Mannose oligosaccharide (MOS) has been shown to promote animal growth, maintain intestinal health, and activate the intestinal immune system. However, the question of whether MOS can stimulate the immune system and alleviate acetylsalicylic acid (ASA)-induced gut damage remains unresolved. The purpose of this study was to investigate the impact of MOS pretreatment on the immunological and anti-inflammatory capabilities of rats with ASA-induced intestinal injury. Thirty-six male Sprague-Dawley rats were divided into 6 groups and were fed with 0 (negative control), 100, 300, 600, and 800 mg/kg·Body weight (BW) of MOS for 3 weeks. From day 8, rats were fed with 200 mg/kg BW of ASA for 14 days to induce intestinal injury. The growth performance, viscera index, serum and intestinal immunity, intestinal inflammation and morphology of ASA-induced intestinal injury rats with or without MOS administration were investigated. In MOS deficient rats, oral treatment of ASA causes severe intestine damage and immunological dysfunction. In a rat model, 600 mg/kg BW MOS can lower the expression of inflammatory markers and effectively increase liver index, serum interleukin-2 (IL-2), lysozyme contents, intestinal secretory immunoglobulin A (sIgA) and mucus volume, intestinal villus height, crypt depth and villus height/crypt depth in comparison to the ASA group. These results imply that providing rats with MOS at the appropriate dosage can significantly improve their immune system and successfully shield the intestines from ASA damage. MOS is therefore expected to be a promising gut immunopotentiator for enhancing intestinal health in animals.
The objective of this study was to investigate the effect of mannose oligosaccharides (MOS) against cadmium (Cd)-induced hepatic oxidative damage and analyze its underlying antioxidant mechanism. Thirty male Sprague-Dawley (SD) rats were randomly divided into five groups: control group and four others treated with cadmium chloride (CdCl2)(2 mg/kg body weight (b.w.)) and different MOS levels at 0, 100, 300, 500 mg/kg b.w.. The results demonstrated that administration of MOS at a dose of 500 mg/kg significantly reduced Cd-induced oxidative damage in rat livers. This was evidenced by an increase in body weight gain (BWG) and thymus index. Addtionally, liver superoxide dismutase (SOD), catalase (CAT) and total antioxidant capacity (T-AOC) activities were significantly improved compared to the group exposed to Cd alone. Conversely, MOS resulted in significant reductions in the liver index, liver malondialdehyde (MDA), hydrogen peroxide (H2O2), glutathione (GSH), and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels Morphological analysis showed that MOS ameliorated Cd-induced histopathology of the rat liver. Notably, Nrf2 gene expression levels increased, while heme oxygenase 1 (HO-1) and quinone xidoreductase 1 (NQO1) mRNA levels decreased in the MOS group. In conclusion, MOS effectively attenuate Cd-induced oxidative damage in rat liver and the Nrf2 signaling pathway is involved in this process. This study provides valuable insights for the implementation of MOS applications in livestock and poultry production.
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