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GUT:韩国发现引发酒精性肝损坏的蛋白质和抑制物质

2013-08-01 科技部 科技部

据韩国未来创造科学部消息,全南大学崔兴植教授和韩国生命工学研究院李哲浩博士带领的研究小组发现了在酒精性肝损坏过程中发挥核心作用的蛋白质和可以抑制这种蛋白质的物质,这为研发治疗酒精性肝损坏的药物带来了希望。 消息指出,若持续摄入酒精可引发脂肪肝或酒精性肝炎,炎症恶化时可出现肝硬化现象。研究人员虽已查出酒精在分解过程中形成的自由基(机体氧化反应中产生的有害化合物)是损害肝脏的原因,但没有找到发挥核心

据韩国未来创造科学部消息,全南大学崔兴植教授和韩国生命工学研究院李哲浩博士带领的研究小组发现了在酒精性肝损坏过程中发挥核心作用的蛋白质和可以抑制这种蛋白质的物质,这为研发治疗酒精性肝损坏的药物带来了希望。

消息指出,若持续摄入酒精可引发脂肪肝或酒精性肝炎,炎症恶化时可出现肝硬化现象。研究人员虽已查出酒精在分解过程中形成的自由基(机体氧化反应中产生的有害化合物)是损害肝脏的原因,但没有找到发挥核心作用的蛋白质。

该研究小组在给实验鼠持续注入酒精成分后发现,雌激素受体相关受体(ERRγ)的形成增多,而这个受体促进酒精分解酶的形成,从而形成了自由基。

研究小组还找到了以ERRγ为目标的低分子物质GSK5182,这种物质可以抑制ERRγ的转录。研究小组给实验鼠注入酒精和GSK5182后发现,自由基的形成受到了阻碍,肝损坏也得到了扼制。崔兴植教授表示,GSK5182有可能成为开发治疗酒精性肝损坏药物的候选物质。

这一研究结果已于本月6日表发于国际学术期刊Gut的网络版上。

覆盖

Kim DK, Kim YH, Jang HH, Park J, Kim JR, Koh M, Jeong WI, Koo SH, Park TS, Yun CH, Park SB, Chiang JY, Lee CH, Choi HS.Estrogen-related receptor γ controls hepatic CB1 receptor-mediated CYP2E1 expression and oxidative liver injury by alcohol.Gut. 2013 Jul;62(7):1044-54. doi: 10.1136/gutjnl-2012-303347. Epub 2012 Sep 29.

PMID:
 
23023167

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