College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Life Sci. 2021 Apr 1;270:119138. doi: 10.1016/j.lfs.2021.119138. Epub 2021 Jan 30.
Sodium propionate (SP) has been reported to possess an anti-inflammatory and anti-apoptotic potential by inhibiting certain signaling pathways and helps in reducing the pathological damages of the mammary gland. However, the effects of sodium propionate on attenuating Lipopolysaccharide (LPS)-induced inflammatory condition and cell damage in bovine mammary epithelial cells (bMECs) are not comprehensively studied yet. Therefore, the aim of the current investigation was to evaluate the protective effects of sodium propionate on LPS-induced inflammatory conditions and to clarify the possible underlying molecular mechanism in bMECs.
The effects of increasing doses of SP on LPS-induced inflammation, oxidative stress and apoptosis was studied in vitro. Furthermore, the underlying protective mechanisms of SP on LPS-stimulated bMECs was investigated under different experimental conditions.
The results reveled that increased inflammatory cytokines, chemokines and those of tight junction's mRNA expression was significantly attenuated dose-dependently by propionate. Biochemical analysis revealed that propionate pretreatment modulated the LPS-induced intercellular reactive oxygen species (ROS) accumulation, oxidative and antioxidant factors and apoptosis rate. Furthermore, we investigated that the LPS activated nuclear factor-kB (NF-kB), caspase/Bax apoptotic pathways and Histone deacetylases (HDAC) was significantly attenuated by propionate in bMECs.
Our results suggest that sodium propionate is a potent agent for ameliorating LPS-mediated cellular disruption and limiting detrimental inflammatory responses, partly via maintaining blood milk barrier integrity, inhibiting HDAC activity and NF-kB signaling pathway.
丙酸钠（SP）已被报道通过抑制某些信号通路具有抗炎和抗凋亡作用，并有助于减少乳腺的病理损伤。然而，丙酸钠对减轻脂多糖（LPS）诱导的牛乳腺上皮细胞（bMEC）炎症状态和细胞损伤的影响尚未得到全面研究。因此，本研究旨在评估丙酸钠对 LPS 诱导的炎症状态的保护作用，并阐明其在 bMECs 中的可能潜在分子机制。
在体外研究了不同剂量的 SP 对 LPS 诱导的炎症、氧化应激和凋亡的影响。此外，还在不同实验条件下研究了 SP 对 LPS 刺激的 bMECs 的潜在保护机制。
结果表明，丙酸盐可显著剂量依赖性地减轻 LPS 诱导的促炎细胞因子、趋化因子和紧密连接的 mRNA 表达增加。生化分析表明，丙酸盐预处理可调节 LPS 诱导的细胞内活性氧（ROS）积累、氧化和抗氧化因子以及凋亡率。此外，我们研究了 LPS 激活的核因子-kB（NF-kB）、半胱天冬酶/Bax 凋亡途径和组蛋白去乙酰化酶（HDAC）在 bMECs 中被丙酸盐显著抑制。
我们的结果表明，丙酸钠是一种有效的改善 LPS 介导的细胞破坏和限制有害炎症反应的药物，部分通过维持血液乳屏障的完整性、抑制 HDAC 活性和 NF-kB 信号通路。
