色氨酸-3-乙酸诱导的 TNFα 表达抑制作用不是通过 Caco-2 细胞中 AhR 的激活介导的。
Suppression of TNFα expression induced by indole-3-acetic acid is not mediated by AhR activation in Caco-2 cells.
机构信息
The United Graduate School of Agricultural Sciences, Tottori University, Tottori-Shi, Tottori, Japan.
Graduate School of Life and Environmental Science, Shimane University, Matsue, Shimane, Japan.
出版信息
Biosci Biotechnol Biochem. 2021 Mar 24;85(4):902-906. doi: 10.1093/bbb/zbaa101.
Indole-3-acetic acid (IAA) produced by intestinal bacteria from tryptophan in dietary proteins is considered to suppress the inflammatory response through aryl hydrocarbon receptor (AhR) activation. However, AhR activation was not involved in the downregulation of tumor necrosis factor α (TNFα) expression induced by IAA in Caco-2 cells. The activation of unidentified IAA receptors might attenuate the inflammatory response to TNFα in colorectal cancer cells.
肠道细菌利用膳食蛋白中的色氨酸产生的吲哚-3-乙酸（IAA）被认为通过芳基烃受体（AhR）的激活来抑制炎症反应。然而，IAA 在 Caco-2 细胞中诱导的肿瘤坏死因子 α（TNFα）表达下调不涉及 AhR 的激活。未鉴定的 IAA 受体的激活可能会减弱结直肠癌细胞对 TNFα 的炎症反应。
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