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Lactobacillus intestinalis/Lactobacillus rhamnosus protects against AFB_(1)-induced liver damage:involvement of intestinal mucosal barrier

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摘要 Aflatoxin B1(AFB1)is a widely spread mycotoxin that poses a threat to the healthy to human and animals.The liver is the main target organ for AFB1-induced damage,primarily causing inflammatory injury and oxidative stress.When AFB1 enters the body,it can damage the intestinal barrier function,and its metabolites are transported to the liver.Therefore,the damage to the liver is closely associated with intestinal barrier impairment.Lactobacillus plays a crucial role in mitigating liver damage by improving the intestinal barrier function.In our previous report,we reported that Lactobacillus reduces liver damage caused by AFB1.However,it is still unclear how the intestinal barrier contributes to the protective effects of Lactobacillus against AFB1.To investigate the protective effects and intestinal barrier mechanisms of Lactobacillus intestinals/rhamnosus against AFB1-induced liver damage,we orally administered AFB1 and Lactobacillus intestinals/rhamnosus to male SD rats.Then the body weight,organ index,histopathological changes in the liver and gut,liver and kidney function indicators,intestinal mucosal barrier indicators,serum AFB1 content and inflammatory factors,liver oxidative stress index,and short-chain fatty acids content were analyzed.Our findings demonstrate that exposure to AFB1 resulted in changes in liver histopathology and biochemical functions,altered inflammatory response and oxidative stress,compromised the intestinal mucosal barrier,and induced the accumulation of inflammatory factor and inflammation in the liver.However,supplementation with Lactobacillus intestinals or Lactobacillus rhamnosus significantly prevented AFB1-induced liver injury,alleviated histopathological changes and hepatic injury by the maintenance of intestinal mucosal barrier integrity.
出处 《One Health Advances》 2023年第1期94-105,共12页 全健康进展(英文)
基金 funded by National Natural Science Foundation of China(Beijing,China grant no.32125038 and U20A2062).
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