E Duan, W Gao, C Liu, J Wang, J Wang, L Su, H Qiao, P Wang, J Huang, L Gan
{"title":"甘露寡糖对镉致大鼠肝脏氧化损伤的保护作用。","authors":"E Duan, W Gao, C Liu, J Wang, J Wang, L Su, H Qiao, P Wang, J Huang, L Gan","doi":"10.24425/pjvs.2025.154952","DOIUrl":null,"url":null,"abstract":"<p><p>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. Additionally, 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 oxidoreductase 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.</p>","PeriodicalId":94175,"journal":{"name":"Polish journal of veterinary sciences","volume":"28 2","pages":"311-320"},"PeriodicalIF":1.0000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective effect of mannose oligosaccharides on cadmium-induced hepatic oxidative damage in rats.\",\"authors\":\"E Duan, W Gao, C Liu, J Wang, J Wang, L Su, H Qiao, P Wang, J Huang, L Gan\",\"doi\":\"10.24425/pjvs.2025.154952\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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. Additionally, 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 oxidoreductase 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.</p>\",\"PeriodicalId\":94175,\"journal\":{\"name\":\"Polish journal of veterinary sciences\",\"volume\":\"28 2\",\"pages\":\"311-320\"},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2025-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Polish journal of veterinary sciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.24425/pjvs.2025.154952\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Polish journal of veterinary sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.24425/pjvs.2025.154952","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Protective effect of mannose oligosaccharides on cadmium-induced hepatic oxidative damage in rats.
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. Additionally, 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 oxidoreductase 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.