Institute of Human Nutrition and Food Science, University of Kiel, Hermann-Rodewald-Strasse 6, 24118 Kiel, Germany.
Consiglio per la ricerca in agricoltura e l'analisi dell'economia agraria, Centro di ricerca per le colture industriali, Via Di Corticella 133, Bologna 40128, Italy.
J Nutr Biochem. 2015 Jun;26(6):661-6. doi: 10.1016/j.jnutbio.2015.01.004. Epub 2015 Mar 5.
In this study, the effect of myrosinase-treated glucoerucin (GER+MYR), which releases the isothiocyanate (ITC) erucin, on heme oxygenase 1 (HO-1) gene expression and Nrf2 signaling was investigated in vitro in cultured cells and in vivo in mice. Treatment of HT-29 cells with GER+MYR resulted in a significant increase in the mRNA and protein levels of nuclear Nrf2 and HO-1. GER+MYR was more potent at enhancing the nuclear Nrf2 levels than were the following myrosinase-treated glucosinolates: sinigrin, glucoraphanin and gluconasturtiin, which are the precursors of allyl-ITC, R-sulforaphane and 2-phenylethyl ITC, respectively. GER+MYR also significantly induced HO-1 gene expression in the mouse intestinal mucosae and liver but not in the brain. Mechanistic studies suggest that GER+MYR induces Nrf2 via ERK1/2-, p38- and JNK-dependent signal transduction pathways. The GER+MYR-mediated increase in HO-1 expression is primarily attributable to p38 signaling.
在这项研究中，我们研究了黑芥子酶处理的葡萄糖异硫氰酸盐（GER+MYR）对体外培养的细胞和体内小鼠血红素加氧酶 1（HO-1）基因表达和 Nrf2 信号通路的影响。GER+MYR 处理 HT-29 细胞后，核 Nrf2 和 HO-1 的 mRNA 和蛋白水平显著增加。与黑芥子酶处理的其他芥子油苷相比，GER+MYR 更能增强核 Nrf2 水平：这些芥子油苷分别是丙烯基异硫氰酸酯、萝卜硫素和葡萄糖腈的前体，2-苯乙基异硫氰酸酯。GER+MYR 还能显著诱导小鼠肠道黏膜和肝脏中的 HO-1 基因表达，但不能诱导大脑中的 HO-1 基因表达。机制研究表明，GER+MYR 通过 ERK1/2、p38 和 JNK 依赖性信号转导通路诱导 Nrf2。GER+MYR 介导的 HO-1 表达增加主要归因于 p38 信号通路。
