Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2
Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2
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DOI：
10.1007/s11010-005-9064-8
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发表时间：
2006-04-01
影响因子：
4.3
通讯作者：
Evangelou, Angelos
中科院分区：
文献类型：
--
作者：
Kolettas, Evangelos;Thomas, Christoforos;Evangelou, Angelos
迷迭香酸（RosA）是中草药和药用植物中常见的次生代谢产物，具有抗氧化和抗炎活性。RosA具有抑制Jurkat T细胞增殖和诱导凋亡的作用，但其凋亡机制尚不清楚。RosA通过抑制cyclin D-3和p21（Cip1/Waf1）的表达，上调p27(Kip1)，呈剂量依赖性地抑制Jurkat细胞的增殖。RosA诱导Jurkat细胞凋亡呈剂量依赖性，但不能保护Jurkat细胞免受过氧化氢（H2O2）介导的凋亡。RosA诱导细胞凋亡与抑制Bcl-2相关，而与抑制Bak和PUMA无关。通过改变Bcl-2家族中抗凋亡和促凋亡成员的比例，过表达Bcl-2可以保护Jurkat细胞免受H2O2-和rosa诱导的凋亡。综上所述，RosA通过改变细胞周期蛋白和细胞周期蛋白依赖性激酶抑制剂的表达来抑制Jurkat细胞增殖，并诱导细胞凋亡，这很可能是通过线粒体途径起作用的，不具有抗氧化特性。
Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D-3 and p21(Cip1/Waf1) and up-regulating p27(Kip1). RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.