Department of Food and Nutrition, Eulji University, Seongnam 13135, Republic of Korea.
SG Medical, Seoul, Republic of Korea.
J Microbiol Biotechnol. 2020 Jan 28;30(1):71-78. doi: 10.4014/jmb.1907.07050.
S1 strongly inhibits the expression of interleukin (IL)-6 and IL-1β in lipopolysaccharide-induced peritoneal macrophages by a mechanism for which lactic acid bacteria from kimchi that inhibit tumor necrosis factor-alpha (TNF-κ) were isolated. Therefore, we further evaluated the protective effect of this strain on the colitis mouse model induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS significantly elevated myeloperoxidase (MPO) expression, macroscopic scores, and colon shortening. Oral S1 administration resulted in reduction of TNBS-induced loss in body weight, colon shortening, MPO activity, expression of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB). S1 inhibited the expression of inflammatory cytokines IL-1β, IL-6 and TNF-κ, induced by TNBS, but enhanced IL-10 expression. S1 showed resistance to artificial digestive juices and adherence to intestinal epithelial Caco-2 cells. Thus, S1 may inhibit the NF-κB pathway and be used in functional food to treat colitis.
S1 通过一种机制强烈抑制脂多糖诱导的腹腔巨噬细胞中白细胞介素 (IL)-6 和 IL-1β 的表达，这种机制分离出了抑制肿瘤坏死因子-α (TNF-κ) 的泡菜乳酸菌。因此，我们进一步评估了该菌株对 2,4,6-三硝基苯磺酸 (TNBS) 诱导的结肠炎小鼠模型的保护作用。TNBS 显著升高髓过氧化物酶 (MPO) 表达、宏观评分和结肠缩短。口服 S1 可减少 TNBS 诱导的体重减轻、结肠缩短、MPO 活性、环氧化酶 (COX)-2、诱导型一氧化氮合酶 (iNOS) 和核因子-kappa B (NF-κB) 的表达。S1 抑制了 TNBS 诱导的炎性细胞因子 IL-1β、IL-6 和 TNF-κ 的表达，但增强了 IL-10 的表达。S1 对人工消化液具有抗性，并能黏附于肠上皮 Caco-2 细胞。因此，S1 可能通过抑制 NF-κB 通路，用于治疗结肠炎的功能性食品。
