Study on the regulatory mechanisms of neurodegenelation by tryptophan key enzymes

喹啉酸（QA），色氨酸代谢产物，被观察到增加在大脑中的神经退行性疾病患者。吲哚胺2，3-脱氧酶（IDO）和氨基羧基粘康酸半醛脱羧酶（ACMSD）影响QA的产生。在这项研究中，我们研究了一些食物成分对IDO或ACMSD在小胶质细胞或LPS处理的参与神经退行性疾病发病机制的小鼠中表达的影响。谷物中的多酚抑制小胶质细胞和LPS处理的小鼠脑中的IDO表达。我们的研究结果表明，抑制NF-κ B途径可能部分参与了调节机制的IDO表达的多酚类物质在谷物。我们还发现，植醇降低ACMSD活性，其蛋白和mRNA的表达。这种机制可能是由于激活了PPAR α。一些食物成分可能被认为有助于避免中枢神经系统炎症。

Quinolinic acid (QA), a tryptophan metabolite, was observed to increase in brains of patients with neurodegenerative diseases. Indoleamine 2,3-deoxygenase (IDO) and amino carboxymuconate semialdehyde decarboxylase (ACMSD) affect QA production. In this study, we investigated the effect of some food components on IDO or ACMSD expression in microglial cells or LPS treated mice involved in neurodegenerative disease pathogenesis. Polyphenols in cereals suppressed IDO expression in microglial cells and in brain of LPS treated mice. Our results suggest that inhibition of the NF-kB pathway may be partly involved in the regulatory mechanism of IDO expression by polyphenols in cereals. We also found that phytol decreased ACMSD activity, its protein and mRNA expression. It is possible that this mechanism resulted from the activation of PPAR alpha. Some food components may be considered helpful for avoiding central nervous system inflammation.