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龙牙楤木芽中五种三萜类化合物对人中性粒细胞刺激诱导的超氧化物生成、酪氨酸磷酸化及胞质化合物向细胞膜转位的影响。

Effect of five triterpenoid compounds from the buds of Aralia elata on stimulus-induced superoxide generation, tyrosyl phosphorylation and translocation of cytosolic compounds to the cell membrane in human neutrophils.

作者信息

Zhang Mei, Liu Gang, Tang Shuhan, Song Shaojiang, Yamashita Koichi, Manabe Masanobu, Kodama Hiroyuki

机构信息

Department of Anesthesiology and Critical Care Medicine, Kochi Medical School, Nankoku-shi, Kochi 783-8505, Japan.

出版信息

Planta Med. 2006 Oct;72(13):1216-22. doi: 10.1055/s-2006-951679. Epub 2006 Oct 4.

DOI:10.1055/s-2006-951679
PMID:17021995
Abstract

The buds of Aralia elata (Miq.) Seem (Japanese angelica tree) have long been used as a tonic, antiarthritic and antidiabetic agent in China and Japan. We have isolated five triterpenoids, congmuyanosides A, C, D, echinocystic acid and 3-O-[beta-D-glucopyranosyl(1-->2)-beta-D-glucopyranosyl]-hederagenin from the buds of Aralia elata , and investigated their effects on stimulus-induced superoxide generation in human neutrophils. Congmuyanoside A, echinocystic acid and 3-O-[beta-D-glucopyranosyl(1-->2)-beta-D-glucopyranosyl]-hederagenin suppressed the superoxide generation induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) in a concentration-dependent manner. Congmuyanosides C, D and echinocystic acid significantly suppressed the superoxide generation induced by phorbol 12-myristate 13-acetate (PMA) and arachidonic acid (AA). The compounds also suppressed fMLP- and AA-induced tyrosyl or PMA-induced serine/threonine phosphorylation and translocation of cytosolic compounds, p47 (phox), p67 (phox) and Rac to the cell membrane.

摘要

辽东楤木(Aralia elata (Miq.) Seem,即刺老芽)的芽在中国和日本长期以来被用作滋补品、抗关节炎和抗糖尿病药物。我们从辽东楤木的芽中分离出了五种三萜类化合物,即葱木皂苷A、C、D、紫花前胡酸和3 - O - [β - D - 吡喃葡萄糖基(1→2)-β - D - 吡喃葡萄糖基]-常春藤皂苷元,并研究了它们对人中性粒细胞刺激诱导的超氧化物生成的影响。葱木皂苷A、紫花前胡酸和3 - O - [β - D - 吡喃葡萄糖基(1→2)-β - D - 吡喃葡萄糖基]-常春藤皂苷元以浓度依赖的方式抑制了N - 甲酰 - 甲硫氨酰 - 亮氨酰 - 苯丙氨酸(fMLP)诱导的超氧化物生成。葱木皂苷C、D和紫花前胡酸显著抑制了佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯(PMA)和花生四烯酸(AA)诱导的超氧化物生成。这些化合物还抑制了fMLP和AA诱导的酪氨酸磷酸化或PMA诱导的丝氨酸/苏氨酸磷酸化以及胞质化合物p47(phox)、p67(phox)和Rac向细胞膜的转位。

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