Bifidobacterium lactis attenuates onset of inflammation in a murine model of colitis

AIM: To assess the anti-inflammatory effect of the probiotic Bifidobacterium lactis (B. lactis) in an adoptive transfer model of colitis. METHODS: Donor and recipient mice received either B. lactis or bacterial culture medium as control (deMan Rogosa Sharpe) in drinking water for one week prior to transfer of a mix of naive and regulatory T cells until sacrifice. RESULTS: All recipient mice developed signs of colonic inflammation, but a significant reduction of weight loss was observed in B. lactis-fed recipient mice compared to control mice. Moreover, a trend toward a diminution of mucosal thickness and attenuated epithelial damage was revealed. Colonic expression of pro-inflammatory and T cell markers was significantly reduced in B. lactis-fed recipient mice compared to controls. Concomitantly, forkhead box protein 3, a marker of regulatory T cells, was significantly up-regulated by B. lactis. CONCLUSION: Daily oral administration of B. lactis was able to reduce inflammatory and T cells mediators and to promote regulatory T cells specific markers in a mouse model of colitis.

Cis-hydroxyproline-induced inhibition of pancreatic cancer cell growth is mediated by endoplasmic reticulum stress

瞄准：在老鼠上调查 cis-hydroxyproline (CHP ) 的生物效果，并且检验内在的分子的机制胰腺的癌房间线 DSL6A。方法：DSL6A 房间增长上的 CHP 的效果被使用 BrdU 加入估计。焦点的粘附激酶(FAK ) 的表示被西方的弄污和免疫荧光描绘。endoplasmic 感应(嗯) 应力被使用 RT-PCR 并且为葡萄糖相关的 protein-78 (GRP78 ) 和生长拘捕和 DNA 的西方的弄污调查可诱导的基因(GADD153 ) 。房间生存能力通过基于 DSL6A 房间的减小潜力测量新陈代谢的活动被决定。Apoptosis 被 caspase-3 激活的察觉和多形核白细胞(自动数据处理核糖) 的劈开分析象 DNA laddering 一样的聚合酶(PARP ) 。结果：除了增长的抑制，有 CHP 的孵化从焦点的粘附导致了 FAK 的解朊的劈开和酶的 delocalisation，由房间坚持的损失列在后面。同时，我们能显示出 GRP78 和 GADD153 的增加的表情，显示在 DSL6A 房间线的 ER 压力串联的调停 CHP 的激活。有 CHP 的 DSL6A 房间的延长孵化最后导致了 apoptotic 细胞死亡。在 L 脯氨酸旁边，由一个广谱朊酶禁止者的增加的细胞内部的解朊作用的抑制能在细胞的功能和分子的过程上废除 CHP 的效果。相反，阻碍执行 apoptosis caspases 的活动没在调停 CHP 的房间损坏上有影响。结论：我们的数据建议开始嗯由 CHP 的压力机械导致细胞内部的解朊的进程的激活包括 caspase 独立的 FAK 降级，导致损坏胰腺的癌房间。