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6-(Methylsulfinyl)hexyl isothiocyanate protects acetaldehyde-caused cytotoxicity through the induction of aldehyde dehydrogenase in hepatocytes.
Archives of Biochemistry and Biophysics ( IF 3.8 ) Pub Date : 2020-03-07 , DOI: 10.1016/j.abb.2020.108329 Tomoya Kitakaze 1 , Sihao Yuan 1 , Masako Inoue 1 , Yasukiyo Yoshioka 2 , Yoko Yamashita 1 , Hitoshi Ashida 1
Archives of Biochemistry and Biophysics ( IF 3.8 ) Pub Date : 2020-03-07 , DOI: 10.1016/j.abb.2020.108329 Tomoya Kitakaze 1 , Sihao Yuan 1 , Masako Inoue 1 , Yasukiyo Yoshioka 2 , Yoko Yamashita 1 , Hitoshi Ashida 1
Affiliation
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In the body, alcohol dehydrogenase rapidly converts ethanol to its toxic metabolite, acetaldehyde, which is further metabolized to non-toxic acetic acid by aldehyde dehydrogenase (ALDH). 6-(methylsulfinyl)hexyl isothiocyanate (6-MSITC), a major bioactive compound in Wasabi (Wasabia japonica) has various physiological effects such as anti-oxidative, anti-inflammatory and anti-cancer effects. However, the effect of 6-MSITC on alcohol metabolism has not been studied. In this study, we investigated the effects of 6-MSITC on hepatic ALDH activity and protein expression both in vitro and in vivo. 6-MSITC inhibited ethanol- and acetaldehyde-induced cytotoxicity. Treatment with 6-MSITC to HepG2 cells enhanced ALDH activity through the induction of mitochondrial ALDH2 expression, but not cytosolic ALDH1A1. Knockdown of Nrf2 canceled the 6-MSITC-induced ALDH2 expression, indicating that Nrf2 regulated ALDH2 expression. Moreover, 6-MSITC increased the nuclear translocation of Nrf2 and the expression levels of HO-1 and SOD2, Nrf2-regulated phase II drug-metabolizing enzymes. Oral administration of 6-MSITC increased the mitochondrial ALDH2 activity and its expression in the liver of C57BL/6J mice. These results suggested that 6-MSITC is possible to protect acetaldehyde toxicity in hepatocytes by induction of mitochondrial ALDH2 expression through Nrf2/ARE pathway.
中文翻译：
6-（甲基亚磺酰基）己基异硫氰酸酯通过诱导肝细胞中的醛脱氢酶来保护乙醛引起的细胞毒性。
在体内，乙醇脱氢酶将乙醇迅速转化为有毒代谢产物乙醛，然后再通过醛脱氢酶（ALDH）代谢为无毒乙酸。6-（甲基亚磺酰基）己基异硫氰酸酯（6-MSITC）是芥末（Wasbia japonica）中的主要生物活性化合物，具有多种生理作用，例如抗氧化，抗炎和抗癌作用。然而，尚未研究6-MSITC对酒精代谢的影响。在这项研究中，我们调查了6-MSITC在体外和体内对肝ALDH活性和蛋白质表达的影响。6-MSITC抑制乙醇和乙醛诱导的细胞毒性。用6-MSITC处理HepG2细胞可通过诱导线粒体ALDH2表达增强ALDH活性，但不能诱导胞质ALDH1A1表达。击倒Nrf2取消了6-MSITC诱导的ALDH2表达，表明Nrf2调节了ALDH2表达。此外，6-MSITC增加了Nrf2的核转运以及HO-1和SOD2，Nrf2调节的II期药物代谢酶的表达水平。口服6-MSITC可以增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。口服6-MSITC可增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。口服6-MSITC可增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。
更新日期：2020-03-09
中文翻译：
6-（甲基亚磺酰基）己基异硫氰酸酯通过诱导肝细胞中的醛脱氢酶来保护乙醛引起的细胞毒性。
在体内，乙醇脱氢酶将乙醇迅速转化为有毒代谢产物乙醛，然后再通过醛脱氢酶（ALDH）代谢为无毒乙酸。6-（甲基亚磺酰基）己基异硫氰酸酯（6-MSITC）是芥末（Wasbia japonica）中的主要生物活性化合物，具有多种生理作用，例如抗氧化，抗炎和抗癌作用。然而，尚未研究6-MSITC对酒精代谢的影响。在这项研究中，我们调查了6-MSITC在体外和体内对肝ALDH活性和蛋白质表达的影响。6-MSITC抑制乙醇和乙醛诱导的细胞毒性。用6-MSITC处理HepG2细胞可通过诱导线粒体ALDH2表达增强ALDH活性，但不能诱导胞质ALDH1A1表达。击倒Nrf2取消了6-MSITC诱导的ALDH2表达，表明Nrf2调节了ALDH2表达。此外，6-MSITC增加了Nrf2的核转运以及HO-1和SOD2，Nrf2调节的II期药物代谢酶的表达水平。口服6-MSITC可以增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。口服6-MSITC可增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。口服6-MSITC可增加线粒体ALDH2活性及其在C57BL / 6J小鼠肝脏中的表达。这些结果表明6-MSITC可能通过通过Nrf2 / ARE途径诱导线粒体ALDH2表达来保护肝细胞中乙醛毒性。
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