过度的炎症反应会导致类风湿性关节炎和心血管疾病等各种并发症。因此，我们的研究目标是调查热灭活乳酸杆菌Latilactobacillus sakei CNS001WB和Lactobacillus pentosus WB693是否能够预防炎症反应。当LPS刺激的RAW 264.7细胞接触热灭活的Lact. sakei CNSC001WB或Lact. pentosus WB693时，一氧化氮的产生减少。此外，环氧合酶（COX）-2和促炎细胞因子（如肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β和IL-6）的表达被抑制。在炎症疾病特别是关节炎中起重要作用的前列腺素E2（PGE2）和白三烯B4（LTB4）的表达也减少。此外，这些菌株抑制了核因子-κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号通路，这些通路激活了各种细胞因子和炎症介质。此外，热灭活的Lact. sakei CNSC001WB和Lact. pentosus WB693还抑制了活性氧（ROS）的产生。根据这些结果，我们得出结论：热灭活的Lact. sakei CNSC001WB和Lact. pentosus WB693能够充分抑制炎症反应，具有抗炎潜力。©2023作者，独家授权给Springer Science+Business Media，LLC，Springer Nature的一部分。

Excessive inflammatory results, such as those seen in rheumatoid arthritis and cardiovascular diseases, are known to cause various complications. Therefore, we aimed to investigate whether heat-killed Latilactobacillus sakei CNS001WB and Lactobacillus pentosus WB693 can prevent inflammatory reactions. When LPS-stimulated RAW 264.7 cells were handled with either heat-killed Lact. sakei CNSC001WB or Lact. pentosus WB693, the production of nitric oxide reduced. Furthermore, the expression of cyclooxygenase (COX)-2 and proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, was suppressed. The expression of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4), which play important roles in inflammatory diseases, especially arthritis, was also reduced. Moreover, these strains inhibited nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, which activate various cytokines and inflammatory mediators. Additionally, heat-killed Lact. sakei CNSC001WB and Lact. pentosus WB693 inhibited the reactive oxygen species (ROS) production. Based on these results, we concluded that heat-killed Lact. sakei CNSC001WB and Lact. pentosus WB693 sufficiently inhibited the inflammatory response and may have anti-inflammatory potential.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.