Lee Jeong Min, Hwang Kwon-Tack, Jun Woo Jin, Park Chang-Soo, Lee Myung-Yul
Department of Medical Nutrition, Graduate School of East-West Medical Science and Research Institute of Clinical Nutrition,Kyung Hee University, Yongin 446-701, Korea.
J Microbiol Biotechnol. 2008 Oct;18(10):1683-8.
Lactobacillus casei 3260 (L. casei 3260) was evaluated in relation to the inflammatory response mediated by lipopolysaccharide (LPS)-induced nuclear factor-kappaB (NF-kappaB) and cyclooxygenase-2 (COX-2) expression in Raw264.7 macrophage cells. The treatment of Raw264.7 cells with L. casei 3260 significantly inhibited the secretion of tumor necrosis factor-alpha (TNF-alpha) and prostaglandins E2 (PGE2), followed by suppression of COX-2. To clarify the molecular mechanism, the inhibitory effect of L. casei 3260 on the NF-kappaB signaling pathway was examined based on the luciferase reporter activity. Although the treatment of Raw264.7 cells with L. casei 3260 did not affect the transcriptional activity of NF-kappaB, it did inhibit NF-kappaB activation, as determined by the cytosolic p65 release and degradation of I-kappaBalpha. Therefore, these findings suggest that the suppression of COX-2 through inhibiting the NF-kappaB activation by LPS may be associated with the antiinflammatory effects of L. casei 3260 on Raw264.7 cells.
对干酪乳杆菌3260（L. casei 3260）进行了评估，研究其对脂多糖（LPS）诱导的核因子-κB（NF-κB）介导的炎症反应以及对Raw264.7巨噬细胞中环氧化酶-2（COX-2）表达的影响。用L. casei 3260处理Raw264.7细胞可显著抑制肿瘤坏死因子-α（TNF-α）和前列腺素E2（PGE2）的分泌，随后抑制COX-2。为阐明分子机制，基于荧光素酶报告基因活性检测了L. casei 3260对NF-κB信号通路的抑制作用。虽然用L. casei 3260处理Raw264.7细胞不影响NF-κB的转录活性，但通过胞质p65释放和I-κBα降解测定，其确实抑制了NF-κB的激活。因此，这些发现表明，通过抑制LPS诱导的NF-κB激活来抑制COX-2可能与L. casei 3260对Raw264.7细胞的抗炎作用有关。
