Functional substance search of horticultural products and research of the action mechanism of a functional substance

园艺产品功能性物质搜寻及功能性物质作用机制研究

• 批准号: 16580028
• 负责人: ADACHI Masaru
• 金额: $ 2.24万
• 依托单位: University of Miyazaki
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2004
• 资助国家: 日本
• 起止时间: 2004 至 2006
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16580028/
• 关键词: horticultural crop; bioactive component; antioxidation; Sweetpotato; ポリフェノール; 抗酸化作用; 抗ガン; アポトーシス; HL-60細胞; キンカン; カンショ; Sweetpea; マンゴー

Dihydropyrazine (DHP) species are included in the Maillard reaction intermediates. The Maillard reaction is thought to play a role in the pathophysiology of aging and diabetes. Thus, DHP may be involved in aging and diabetes related diseases, however, there is little reported the biological and physiological roles of DHPs. Moreover, polyphenolics(POPs) as a secondary metabolite in plant, have various physiological functions and play important roles in human nutrition. By using Escherichia coli mutant strains, we observed that cyclohexyl-DHP exposure strongly reduced the survival rate of a cytosolic sodium dodecyl sulfate (SOD)-deficient strain (sodA sodB), significantly reduced the survival rates of DNA repair-deficient strains (recA and uvrB) and mildly reduced the survival rate of a catalase-deficient strain (katE katG) compared with the survival rate of the wild-type strain. Addition of Cu(2+) enhanced the cell killing ability of cyclohexyl-DHP. The frequency of mutations induced by cyclohexyl-DHP increased dose-dependently in the sodA sodB strain. Moreover, cyclohexyl-DHP elevated the protein carbonyl levels in E caoli. We investigated the suppression of the proliferation of selected human cancer cells by phenolic compounds isolated from sweetpotato leaf. Caffeic acid and di-and tricaffeoylquinic acids dose-dependently depressed cancer cell proliferation, and the difference in sensitivity between caffeoylquinic acid derivatives and each kind of cancer cell was observed. Specifically, 3,4,5-tri-O-caffeoylquinic acid effectively depressed the growth of three kinds of cancer cells, and caffeic acid had an exceptionally higher effect against romyelocytic leukemia cells (HL-60) than other di- and tricaffeoylquinic acids.

二氢吡嗪（DHP）物质包括在美拉德反应中间体中。美拉德反应被认为在衰老和糖尿病的病理生理学中起作用。因此，DHP可能参与衰老和糖尿病相关疾病的发生发展，然而，DHP的生物学和生理学作用的报道很少。此外，多酚类化合物作为植物体内的次生代谢产物，具有多种生理功能，在人类营养中发挥着重要作用。通过使用大肠杆菌突变株，我们观察到，环己基-DHP暴露强烈降低了细胞溶质十二烷基硫酸钠（SOD）缺陷株（sodA sodB）的存活率，显着降低了DNA修复缺陷株（recA和uvrB）的存活率，并轻度降低了过氧化氢酶缺陷株（katE katG）的存活率与野生型菌株的存活率相比。Cu（2+）的加入增强了环己基-DHP的细胞杀伤能力。环己基-DHP诱导的突变频率在sodA sodB菌株中呈剂量依赖性增加。此外，环己基-DHP提高蛋白质羰基水平在E草。我们研究了从甘薯叶中分离的酚类化合物对选定的人类癌细胞增殖的抑制作用。咖啡酸和二和三咖啡酰奎宁酸剂量依赖性地抑制癌细胞增殖，并观察到咖啡酰奎宁酸衍生物和每种癌细胞之间的敏感性差异。具体而言，3，4，5-三-O-咖啡酰奎宁酸有效地抑制了三种癌细胞的生长，并且咖啡酸对骨髓性白血病细胞（HL-60）的作用比其他二-和三-咖啡酰奎宁酸高得多。

项目成果

Oxidative stress induced by a dihydropyrazine derivative

二氢吡嗪衍生物诱导的氧化应激

• 发表时间: 2009
• 期刊: Biol.Pharm.Bull. 32
• 作者: Takechi,S.;Nakahara,K.;Adachi,M.;Yamaguchi,T.
• 通讯作者: Yamaguchi,T.

Growth inhibition and mutagenesis induced in Escherichia coli by dihydropyrazines with DNA strand-cleaving activity.

具有 DNA 链切割活性的二氢吡嗪可诱导大肠杆菌生长抑制和诱变。

• 发表时间: 2004
• 期刊: Mutation Research 560
• 作者: Takechi;S.;Yamaguchi;T.;Nomura;H.;Minematsu;T.;Nakayama;T.
• 通讯作者: T.

Anti tri-ο-caffeoylquinic acid polyclonal antibody. I.Preparation and properties of polyclonal antibodies tocovalently coupled tri-ο-caffeoylquinic acid-albumin

抗三邻咖啡酰奎尼酸多克隆抗体一、共价偶联三邻咖啡酰奎尼酸白蛋白多克隆抗体的制备及性质。

• 发表时间: 2008
• 期刊: Acta Horticulturae 770
• 作者: Kurata R.;Adachi M.;Kurata,H.;Yoshimoto M.
• 通讯作者: Yoshimoto M.

Growth suppression of human cancer cells by polyphenolics from sweetpotato(IPoRoea batatas L.)leaves

甘薯 (IPoRoea batatas L.) 叶多酚类化合物抑制人类癌细胞生长

• 发表时间: 2007
• 期刊: J.Agr.Food Chem. 55・1
• 作者: Kurata R.;Adachi M.;Yamakawa O.;Yoshimoto M.
• 通讯作者: Yoshimoto M.

Physiological active compound in petals of sweet pea(Lathyrus odoratus L.)flower

香豌豆花花瓣中的生理活性化合物

• 发表时间: 2004
• 期刊: Pol.Commun. 22
• 作者: Kurata;H.;Adachi;M.;Kurata R.;Yoshimoto M.;Nakamura;K.;Hattanda;N.;Nagata;R.;Todoroki;A.;Tatsumi;Y.;Takechi;S.
• 通讯作者: S.