Anti-inflammatory effects of Lactobacillus brevis K65 on RAW 264.7 cells and in mice with dextran sulphate sodium-induced ulcerative colitis

作者：Liu Y W; Ong W K; Su Y W; Hsu C C; Cheng T H^*; Tsai Y C^*

来源：Beneficial Microbes, 2016, 7(3): 387-396.

DOI：10.3920/BM2015.0109

• Lactobacillus brevis K65
• lactic acid bacteria
• dextran sulphate sodium
• ulcerative colitis
• anti-inflammatory

Lactic acid bacteria (LAB) with anti-inflammatory effects may be beneficial to the prevention or treatment for inflammation-related diseases, such as inflammatory bowel diseases. In an in vitro assay, heat-killed Lactobacillus brevis K65 (K65) reduced lipopolysaccharide-induced production of nitric oxide, tumour necrosis factor (TNF)-alpha and prostaglandin E-2 in RAW 264.7 cells. In RAW 264.7 cells stably expressing an ind=ucible nitric oxide synthase (iNOS) reporter, viable K65 showed greater inhibition of iNOS production than its heat-killed form. In order to further examine the in vivo anti-inflammatory effect of K65, viable K65 was orally administered to BALB/c mice before and during the period of dextran sulphate sodium (DSS)-induced ulcerative colitis (UC). K65 improved UC symptoms, including reduced the levels of the pro-inflammatory cytokines, TNF-alpha, interleukin (IL)-6 and IL-1 beta, and lowered the activity of myeloperoxidase. Furthermore, K65 inhibited TNF-alpha, cyclo-oxygenase 2, forkhead box P3, and Toll-like receptor 4 mRNA expression in the colonic tissue of DSS-induced UC mice. Taken together, K65, a LAB with in vitro anti-inflammatory activity showed preventive effects on mice with DSS-induced UC by lowering the expression of inflammatory molecules.

• 出版日期2016