Increases in Tryptophan-kynurenine pathway metabolism following interferon-induced depression

干扰素诱导的抑郁症后色氨酸-犬尿氨酸途径代谢增加

• 批准号: 23390149
• 负责人: SAITO KUNIAKI
• 金额: $ 11.98万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23390149/
• 关键词: サイトカイン; インターフェロン; トリプトファン; IDO; 抑うつ; ウイルス性肝炎; コンパニオン診断; 病態検査学; 酵素誘導; うつ病

Increases in L-tryptophhn (TRP) to L-kynurenine (KYN) pathway metabolism were found in interferon (IFN) treated-HCV patients with depressive symptoms. Further, mice with Interferon (IFN) gene transfection induced indoleamine 2,3-dioxygenase (IDO1) , resulting marked increase in TRP to KYN pathway metabolites, which well correlated with depression. The blockade of IDO1 activation prevented the development of depressive-like behavior.

在干扰素（IFN）治疗的有抑郁症状的HCV患者中发现了L-犬尿氨酸（TRP）至L-犬尿氨酸（KYN）途径代谢的增加。此外，干扰素（IFN）基因转染的小鼠诱导吲哚胺2，3-双加氧酶（IDO 1），导致TRP至KYN途径代谢物的显著增加，这与抑郁症密切相关。IDO 1激活的阻断阻止了抑郁样行为的发展。

项目成果

Acquired resistance of leukemic cells to AraC is associated with the upregulation of aldehyde dehydrogenase 1 family member A2.

获得的白血病细胞对ARAC的耐药性与醛脱氢酶1家族成员A2的上调有关。

• DOI: 10.1016/j.exphem.2013.03.004
• 发表时间: 2013-07
• 期刊: EXPERIMENTAL HEMATOLOGY
• 影响因子: 2.6
• 作者: Kawasoe, Misaki;Yamamoto, Yasuko;Okawa, Katsuya;Funato, Tadao;Takeda, Mayu;Hara, Takeshi;Tsurumi, Hisashi;Moriwaki, Hisataka;Arioka, Yuko;Takemura, Masao;Matsunami, Hidetoshi;Markey, Sanford P.;Saito, Kuniaki
• 通讯作者: Saito, Kuniaki

Labdane-type diterpene, constituent from myoga which are traditional Japanese food inhibit enzyme activity and gene expression of in doleamine 2, 3-dioxygenase 1

拉丹烷型二萜，来自日本传统食品 myoga 的成分，抑制多尔胺 2, 3-双加氧酶 1 的酶活性和基因表达

• 发表时间: 2013
• 作者: Imai;R Yamamoto;Y Yamamoto;Y Katayan agi;R Fukutomi;M Abe;Y Ozawa;K Saito
• 通讯作者: K Saito

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• DOI: 10.3892/ol.2012.761
• 发表时间: 2012-09
• 期刊: Oncology letters
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• 发表时间: 2013
• 作者: Tohru Takemasa;Yousuke Abe;Chiaki Kumagai;Hidenori Kiyosawa;Saito,K
• 通讯作者: Saito,K