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人参根中人参皂苷对人中性粒细胞刺激诱导的超氧化物生成、酪氨酸或丝氨酸/苏氨酸磷酸化以及胞质化合物向质膜转位的抑制作用。

Inhibitory effects of ginsenosides from the root of Panax ginseng on stimulus-induced superoxide generation, tyrosyl or serine/threonine phosphorylation, and translocation of cytosolic compounds to plasma membrane in human neutrophils.

作者信息

He Wenfei, Liu Gang, Chen Xin, Lu Jincai, Abe Hidehiro, Huang Kexin, Manabe Masanobu, Kodama Hiroyuki

机构信息

Department of Anesthesiology and Critical Care Medicine, Kochi Medical School, Nankoku-city, Kochi, Japan.

出版信息

J Agric Food Chem. 2008 Mar 26;56(6):1921-7. doi: 10.1021/jf073364k. Epub 2008 Feb 26.

DOI:10.1021/jf073364k
PMID:18298074
Abstract

The effects of five ginsenosides (G-Rh2, -Rd, -Rb1, -Rb2, -Rh1) isolated from the root of Panax gingseng on stimulus-induced superoxide generation in human neutrophils were evaluated by measuring the reduction of ferricytochrome c. The tyrosyl or serine/threonine phosphorylation of neutrophil proteins and translocation of p47phox, p67phox, and Rac to the plasma membrane were detected using specific monoclonal antibodies. G-Rh2 significantly suppressed superoxide generation induced by N-formylmethionyl-leucylphenylalanine (fMLP), phorbol 12-myristate 13-acetate (PMA), and arachidonic acid (AA) in a concentration-dependent manner. G-Rh1 showed a comparably lower suppression on fMLP-induced superoxide generation. G-Rd, -Rb1, and -Rb2 also suppressed AA-induced superoxide generation in high concentrations. G-Rd and G-Rb1 showed no effect on fMLP- and PMA-induced superoxide generation. FMLP-, PMA-, and AA-induced tyrosyl or serine/threonine phosphorylation and translocation of p47phox, p67phox, and Rac to the plasma membrane were in parallel with the suppression of the stimulus-induced superoxide generation.

摘要

通过测量高铁细胞色素c的还原,评估了从人参根中分离出的五种人参皂苷(G-Rh2、-Rd、-Rb1、-Rb2、-Rh1)对人中性粒细胞刺激诱导的超氧化物生成的影响。使用特异性单克隆抗体检测中性粒细胞蛋白的酪氨酸或丝氨酸/苏氨酸磷酸化以及p47phox、p67phox和Rac向质膜的转位。G-Rh2以浓度依赖性方式显著抑制了由N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(fMLP)、佛波酯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。G-Rh1对fMLP诱导的超氧化物生成的抑制作用相对较低。G-Rd、-Rb1和-Rb2在高浓度时也抑制了AA诱导的超氧化物生成。G-Rd和G-Rb1对fMLP和PMA诱导的超氧化物生成没有影响。FMLP、PMA和AA诱导的酪氨酸或丝氨酸/苏氨酸磷酸化以及p47phox、p67phox和Rac向质膜的转位与刺激诱导的超氧化物生成的抑制作用平行。

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