In vitro study of sodium butyrate on soyasaponin challenged intestinal epithelial cells of turbot (Scophthalmus maximus L.) refer to inflammation, apoptosis and antioxidant enzymes

The study is aimed to investigate the protective effect and potential mechanisms of sodium butyrate (NaBT) on soyasaponins (SA) induced intestinal epithelial cells (IECs) injury in vitro. The primary IECs of turbot were developed and treated with 0.4, 1 and 4 mM NaBT in the presence of 0.4 mg/mL SA...

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Bibliographic Details
Published in:Fish and Shellfish Immunology Reports
Main Authors: Guijuan Yu, Weihao Ou, Qinghui Ai, Wenbing Zhang, Kangsen Mai, Yanjiao Zhang
Format: Article in Journal/Newspaper
Language:English
Published: Elsevier 2021
Subjects:
Sodium butyrate
Soyasaponins
Inflammation
Apoptosis
MAPKs
Turbot
Zoology
QL1-991
Scophthalmus maximus
Online Access:https://doi.org/10.1016/j.fsirep.2021.100031
https://doaj.org/article/dbc1f0afb0844a518edd9a54047e9bd6
Description
Summary:The study is aimed to investigate the protective effect and potential mechanisms of sodium butyrate (NaBT) on soyasaponins (SA) induced intestinal epithelial cells (IECs) injury in vitro. The primary IECs of turbot were developed and treated with 0.4, 1 and 4 mM NaBT in the presence of 0.4 mg/mL SA for 6 h to explore the protective effects of NaBT. The results showed that the addition of NaBT significantly down-regulated gene expression of inflammatory cytokine TNF-α, IL-1β and IL-8, pro-apoptosis relevant gene BAX, caspase-3, caspase-7 and caspase-9 induced by SA, while up-regulated anti-apoptosis gene Bcl-2. SA stimulation did not induce reactive oxygen species production, but elevated gene expression of antioxidant enzyme heme oxygenase-1 and superoxide dismutase. Moreover, the gene expression of those antioxidant enzyme was further up-regulated in NaBT groups. Furthermore, NaBT supplementation decreased the acid phosphatase and alkaline phosphatase activities and suppressed phosphorylation of p38 and c-Jun N-terminal kinase (JNK). In conclusion, NaBT could mitigate SA-induced inflammation and apoptosis and elevate gene expression of antioxidant enzymes on IECs of turbot and p38 and JNK signaling pathway participated in those processes.

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