To evaluate the effects of lactic acid bacteria (LAB) in inflammatory bowel diseases (IBD), we measured the inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against the glycosaminoglycan (GAG) degradation by intestinal bacteria. Bifidobacterium longum HY...
To evaluate the effects of lactic acid bacteria (LAB) in inflammatory bowel diseases (IBD), we measured the inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against the glycosaminoglycan (GAG) degradation by intestinal bacteria. Bifidobacterium longum HY8004 and Lactobacillus plantarum AK8-4 exhibited the most potent inhibition. These LAB inhibited colon shortening and myeloperoxidase production in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitic mice. These LAB also blocked the expression of the proinflammatory cytokines, IL-$1{\beta}$ and TNF-$\alpha$, as well as of COX-2, in the colon. LAB also blocked activation of the transcription factor, NF-${\kappa}B$, and expression of TLR-4 induced by TNBS. In addition, LAB reduced the TNBS-induced bacterial degradation activities of chondroitin sulfate and hyaluronic acid. These findings suggest that GAG degradation-inhibitory LAB may improve colitis by inhibiting inflammatory cytokine expression via TLR-4-linked NF-${\kappa}B$ activation and by inhibiting intestinal bacterial GAG degradation.
To evaluate the effects of lactic acid bacteria (LAB) in inflammatory bowel diseases (IBD), we measured the inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against the glycosaminoglycan (GAG) degradation by intestinal bacteria. Bifidobacterium longum HY8004 and Lactobacillus plantarum AK8-4 exhibited the most potent inhibition. These LAB inhibited colon shortening and myeloperoxidase production in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitic mice. These LAB also blocked the expression of the proinflammatory cytokines, IL-$1{\beta}$ and TNF-$\alpha$, as well as of COX-2, in the colon. LAB also blocked activation of the transcription factor, NF-${\kappa}B$, and expression of TLR-4 induced by TNBS. In addition, LAB reduced the TNBS-induced bacterial degradation activities of chondroitin sulfate and hyaluronic acid. These findings suggest that GAG degradation-inhibitory LAB may improve colitis by inhibiting inflammatory cytokine expression via TLR-4-linked NF-${\kappa}B$ activation and by inhibiting intestinal bacterial GAG degradation.
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제안 방법
The effects of LAB in fecal chondroitin degradation (A), hyaluronidase degradation (B), and tryptophanase (C), and 0- glucuronidase (D) activities in TNBS-induced colitis mice. Test agents (N, normal group treated with vehicle alone; C, TNBS-treated control group; Bl, 50 ㎎/㎏ Bifidobacterium longum HY8004, and TNBS; B2, 100 ㎎/㎏ Bifidobacterium HY8004, and TNBS; LI, 50 ㎎/㎏ Lactobacillus plantarum AK8-4, and TNBS; L2, 100 ㎎/㎏ Lactobacillus AK8-4, and TNBS) were orally administered beginining 3 days prior to TNBS treatment. #Significantly different vs.
The LAB (50 ㎎/㎏ or 100 ㎎/㎏ of Lactobacillus AK8-4 or 50 m以kg or 100 ㎎/㎏ of Bifidobacterium HY8004) were orally administered once a day, beginning 3 days before TNBS treatment until the day before sacrifice. The mice were anesthetized with ether and sacrificed on the 3 rd day after TNBS administration. The colon was quickly removed, opened longitudinally, gently cleared of stool, and used for further study.
Effect of LAB on the protein expression of TLR-4 and COX-2 and the activation of the transcription factor NF-kB (A) and inflammatory cytokines (B) in TNBS-induced colitis in mice. The test agents (N, normal group treated with vehicle alone; C, TNBS- treated control group; Bl, 50 ㎎/㎏Bifidobacterium longum HY8004, and TNBS; B2, 100 ㎎/㎏ Bifidobacterium HY8004, and TNBS; LI, 50 ㎎/㎏ Lactobacillus plantarum AK8-4, and TNBS; L2, 100 ㎎/㎏ Lactobacillus AK8-4, and TNBS) were orally administered beginning 3 days prior to TNBS treatment. The mice were anesthetized and killed following treatment.
데이터처리
Statistical significance was analyzed using one-way ANOVA followed by a Student-Newman-Keuls test.
성능/효과
2). Bifidobacterium HY8004 and Lactobacillus AK8N at 100 ㎎/㎏ inhibited IL-1 μ and TNF-a expression by 78% and 74% and by 84% and 68%, respectively. TNBS also increased the activation ofNF-KB, which regulates the expression ofIL-ip, TNF-a [15], and TLR-4, a potential mediator ofLPS signaling [24], Oral administration of LAB inhibited the activation ofNF-KB and TLR-4 expressions.
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