Abstract

The present study investigated the anti-inflammatory effects and potential mechanisms of sodium butyrate (SB) in bovine embryo tracheal cells (EBTr) stimulated with lipopolysaccharide (LPS). EBTr were exposed to either 1 mmol/L SB for 18 h for the SB group (SB) or to 0.4 μg/mL LPS for 6 h for the LPS group (LPS). PBS was added to EBTr for a control group (CON). EBTr were pretreated with SB for 18 h followed by 6 h of LPS stimulation for the LSB group (LSB). Results showed that with LPS stimulation, the gene expression of TLR4, NF-κB, IL6, and IL8, as well as cytokine production of IL6 and TNF-α, were significantly increased compared with the CON group. In contrast, protein expression of IL10 was decreased. However, these inflammatory effects induced by LPS were reversed in the LSB group. Compared with the CON group, protein expression of TLR4, phospho-NF-κB p65, phospho-IκBα, and IL1α were increased in the LPS group and these were decreased in the LSB group. Similarly, increased nuclear translocation of phospho-NF-κB p65 in the LPS group was suppressed with SB pretreatment. In conclusion, SB can reduce inflammation induced by LPS in EBTr, and this positive effect is mediated through the TLR4 and NF-κB signaling pathway.

摘要

本研究调查了丁酸钠 (SB) 在用脂多糖 (LPS) 刺激的牛胚胎气管细胞 (EBTr) 中的抗炎作用和潜在机制。对于 SB 组 (SB)，EBTr 暴露于 1 mmol/L SB 18 小时，对于 LPS 组 (LPS)，暴露于 0.4 μg/mL LPS 6 小时。将 PBS 添加到 EBTr 中作为对照组 (CON)。EBTr 用 SB 预处理 18 小时，然后对 LSB 组 (LSB) 进行 6 小时的 LPS 刺激。结果显示，与 CON 组相比，在 LPS 刺激下，TLR4、NF-κB、IL6 和 IL8 的基因表达以及 IL6 和 TNF-α 的细胞因子产生显着增加。相反，IL10 的蛋白表达降低。然而，这些由 LPS 诱导的炎症作用在 LSB 组中被逆转。与CON组相比，TLR4蛋白表达，磷酸化 NF-κB p65、磷酸化 IκBα 和 IL1α 在 LPS 组中增加，而在 LSB 组中减少。类似地，LPS 组中磷酸化 NF-κB p65 的核转位增加被 SB 预处理抑制。总之，SB 可以减少 EBTr 中 LPS 诱导的炎症，这种积极作用是通过 TLR4 和 NF-κB 信号通路介导的。