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Fish Shellfish Immunol ; 130: 428-435, 2022 Nov.
Article in English | MEDLINE | ID: mdl-36176225

ABSTRACT

Yeast culture (YC), as a member of probiotics family is a natural product produced from yeast fermentation, affects of improving immunity. However, the intestine and liver injury and immunosuppression mechanism caused by SBA in fish are unclear and more functions of YC supplement in the diet need to be developed. Soybean agglutinin (SBA) is an anti-nutritional factor in soybean and leads to growth-inhibitory effect in feeding of the high proportion of soybean meal replacing fish meal (FM). Therefore, one hundred and thirty-five Pseudobagrus ussuriensis (6.5 ± 0.27 g) were randomly selected and divided into three groups (Control, SBA and YC+SBA groups). For the model, fish were fed with 2% YC for 8 weeks and then given intragastric administration of 0.2-mL SBA solution for 20 days. The results showed that SBA damaged the immune and antioxidant capacity, causing an inflammatory reaction, leading to abnormal expression of cytokines in the intestine and liver of Pseudobagrus ussuriensis. YC could effectively attenuate intestinal and liver damage and downregulate the TLR2/MyD88/NF-κB signaling pathway and suppress oxidative stress in Pseudobagrus ussuriensis. Besides, YC had obvious immune advantage, which could improve the immune ability. In summary, these results showed that YC could reduce immunosuppression and intestinal-liver injury by inhibiting the TLR2/MyD88/NF-κB signal pathway and oxidative stress induced by SBA. This study provided some explanations for the problems of fish diet caused by anti-nutritional factors from soybean meal and provided a theoretical basis for the function development of YC in aquaculture.


Subject(s)
Biological Products , Catfishes , Animal Feed/analysis , Animals , Antioxidants/pharmacology , Catfishes/metabolism , Cytokines/metabolism , Diet/veterinary , Intestines , Myeloid Differentiation Factor 88/metabolism , NF-kappa B/metabolism , Signal Transduction , Glycine max/metabolism , Toll-Like Receptor 2/metabolism
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