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首页> 外文期刊>The Journal of Nutritional Biochemistry >Dietary vitamin B6 intake modulates colonic inflammation in the IL10-/- model of inflammatory bowel disease.
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Dietary vitamin B6 intake modulates colonic inflammation in the IL10-/- model of inflammatory bowel disease.

机译：饮食中维生素B 6 的摄入可调节炎症性肠病IL10 -//-模型中的结肠炎症。

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Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5'-phosphate (PLP) <20 nmol/L] is observed in 19-27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10-/- (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNF alpha, IL-6, IFN- gamma, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation
机译：维生素B 6 的生物活性形式Pyridoxal-5-phosphate是140多种生化反应的辅助因子。尽管很少出现严重的维生素B 6 缺乏症，但在美国19％至27％的人群中观察到轻度的不足[血浆吡x醛5'-磷酸盐（PLP）<20 nmol / L]。血浆PLP浓度与炎症标记（例如C反应蛋白）成反比。此外，在患有炎症性疾病的患者中血浆PLP降低，而在炎症性肠病（IBD）的情况中，活动性与静止性疾病患者的血浆PLP降低更多。限制B 6 的摄入可减轻小鼠的IBD病理。但是，补充的作用尚不清楚。因此，我们寻求确定轻度不足和适度补充B6对结肠炎症严重程度的影响。向断奶的IL-10 -/-（肝炎性肝炎阳性）小鼠喂食含有0.5（不足），6.0（充分）或24（补充）mg / kg盐酸吡ido醇的饮食12周，然后进行评估用于结肠炎的组织学和分子标记。高血浆PLP和低血浆PLP均与结肠中炎症分子的显着抑制（TNFα，IL-6，IFN-γ，COX-2和iNOS表达）和组织学标记有关。 PLP是通过S1P裂解酶分解1型鞘氨醇（S1P）趋化脂质所必需的。结肠中S1P和PLP的浓度呈显着负相关。如果得到证实，补充维生素B6可能会为IBD的管理提供额外的工具。尽管在许多反应中都需要B6，但其在S1P分解中的作用可能解释了PLP与炎症之间的两相关系。

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