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Sodium butyrate improves antioxidant stability in sub-acute ruminal acidosis in dairy goats

BACKGROUND: Currently, little is known about the effect of sodium butyrate (NaB) on oxidative stress following grain-induced sub-acute ruminal acidosis in dairy goats. In the present study, 18 lactating dairy goats implanted with a ruminal cannula and permanent indwelling catheters in the portal and...

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Detalles Bibliográficos
Autores principales: Ma, Nana, Abaker, Juma Ahamed, Bilal, Muhammad Shahid, Dai, Hongyu, Shen, Xiangzhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131738/
https://www.ncbi.nlm.nih.gov/pubmed/30200953
http://dx.doi.org/10.1186/s12917-018-1591-0
Descripción
Sumario:BACKGROUND: Currently, little is known about the effect of sodium butyrate (NaB) on oxidative stress following grain-induced sub-acute ruminal acidosis in dairy goats. In the present study, 18 lactating dairy goats implanted with a ruminal cannula and permanent indwelling catheters in the portal and hepatic veins were randomly allocated into 3 treatment groups over 20 weeks: low grain (LG, 40% grain; n = 6), high grain (HG, 60% grain; n = 6) and high grain with sodium butyrate (HG + NaB, 60% grain + NaB; n = 6). RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet. The mRNA expression of UGT1A1, NQO1, MGST3, and Nrf2, as well as total Nrf2 protein levels were increased in goats fed the HG + NaB diet. CONCLUSIONS: Our study indicates that sodium butyrate could improve the oxidative status in sub-acute ruminal acidosis through the partial activation of Nrf2-dependent genes.