In vitro study of sodium butyrate on soyasaponin challenged intestinal epithelial cells of turbot (Scophthalmus maximus L.) refer to inflammation, apoptosis and antioxidant enzymes
Guijuan Yu , Weihao Ou , Qinghui Ai , Wenbing Zhang , Kangsen Mai , Yanjiao Zhang
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引用次数: 7
Abstract
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.
本研究旨在探讨丁酸钠(NaBT)对大豆皂苷(SA)诱导的肠上皮细胞(IECs)损伤的保护作用及其可能机制。在0.4 mg/mL SA的条件下,分别用0.4、1和4 mM NaBT培养大菱鲆初代IECs,观察NaBT对IECs的保护作用。结果显示,NaBT的加入显著下调SA诱导的炎性细胞因子TNF-α、IL-1β、IL-8、促凋亡相关基因BAX、caspase-3、caspase-7、caspase-9的基因表达,上调抗凋亡基因Bcl-2的表达。SA刺激不诱导活性氧产生,但提高了抗氧化酶血红素加氧酶-1和超氧化物歧化酶的基因表达。此外,NaBT组这些抗氧化酶的基因表达进一步上调。此外,添加NaBT降低了酸性磷酸酶和碱性磷酸酶的活性,抑制了p38和c-Jun n -末端激酶(JNK)的磷酸化。由此可见,NaBT可减轻sa诱导的炎症和凋亡,提高大比鲆IECs抗氧化酶基因表达,p38和JNK信号通路参与了这些过程。