Department of Alternative Medicine and Bioregulation, Faculty of Medicine and Department of Microbiology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi Yamanashi, Japan.
Evid Based Complement Alternat Med. 2007 Mar;4(1):83-94. doi: 10.1093/ecam/nel059. Epub 2006 Sep 11.
We examined the effects of hemicellulase-treated Agaricus blazei (AB fraction H, ABH) on growth of several tumor cell lines. ABH inhibited the proliferation of some cell lines without cytotoxic effects. It markedly prolonged the S phase of the cell cycle. ABH also induced mitochondria-mediated apoptosis in different cell lines. However, it had no impact on the growth of other cell lines. ABH induced strong activation of p38 mitogen-activated protein kinase (MAPK) in the cells in which it evoked apoptosis. On the other hand, ABH showed only a weak p38 activation effect in those cell lines in which it delayed cell cycle progression with little induction of apoptosis. However, p38 MAPK-specific inhibitor inhibited both ABH-induced effects, and ABH also caused apoptosis in the latter cells under conditions of high p38 MAPK activity induced by combined treatment with TNF-alpha. These results indicate that the responsiveness of p38 MAPK to ABH, which differs between cell lines, determines subsequent cellular responses on cell growth.
我们研究了半纤维素酶处理的姬松茸（AB 部分 H，ABH）对几种肿瘤细胞系生长的影响。ABH 抑制了一些细胞系的增殖而没有细胞毒性作用。它显著延长了细胞周期的 S 期。ABH 还诱导不同细胞系中线粒体介导的细胞凋亡。然而，它对其他细胞系的生长没有影响。ABH 在诱导细胞凋亡的细胞中强烈激活了 p38 丝裂原激活蛋白激酶（MAPK）。另一方面，ABH 仅在那些其诱导细胞周期停滞而很少诱导细胞凋亡的细胞系中表现出较弱的 p38 激活作用。然而，p38 MAPK 特异性抑制剂抑制了 ABH 诱导的这两种作用，并且在 TNF-α联合处理诱导高 p38 MAPK 活性的情况下，ABH 也引起了后一种细胞的细胞凋亡。这些结果表明，p38 MAPK 对 ABH 的反应性在细胞系之间存在差异，决定了随后的细胞对细胞生长的反应。
