Ginsenoside Rh2 induces apoptosis independently of Bcl-2, Bcl-xL or Bax in C6Bu-1 cells
Ginsenoside Rh2 induces apoptosis independently of Bcl-2, Bcl-xL or Bax in C6Bu-1 cells
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DOI：
10.1007/bf02979151
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发表时间：
1999-10-01
影响因子：
6.7
通讯作者：
Park, JD
中科院分区：
文献类型：
--
作者：
Kim, YS;Jin, SH;Park, JD
在人参皂苷Rh2处理的大鼠胶质瘤C6Bu-1细胞中，通过电子显微镜证实细胞凋亡的形态学变化，例如细胞皱缩、染色质浓缩和固缩。为了评估人参皂苷Rh2诱导细胞凋亡是否是由Bcl-2家族成员介导的，我们首先建立了过表达Bcl-2的C6Bu-1细胞。结果表明，人参皂苷 Rh2 处理的 C6Bu-1 细胞中 Bcl-2、Bcl-x(L) 和 Bax 的表达没有改变。 Bcl-2 过表达 C6Bu-1 细胞未能阻止人参皂苷 Rh2 诱导的细胞死亡。这些结果表明，C6Bu-1 细胞中存在其他凋亡途径，需要人参皂苷 Rh2 诱导凋亡，而不是通过 Bcl-2、Bcl-x(L) 或 Bax 途径。
In ginsenoside Rh2-treated rat glioma C6Bu-1 cells, apoptotic morphological changes, such as cell shrinkage, chromatin condensation and pyknosis were confirmed by means of electron microscopy. To evaluate whether induction of apoptosis by ginsenoside Rh2 is mediated by the members of Bcl-2 family, we first established C6Bu-1 cells overexpressing Bcl-2. It was demonstrated that the expression of Bcl-2, Bcl-x(L) and Bax was not altered in ginsenoside Rh2-treated C6Bu-1 cells. Bcl-2 overexpressing C6Bu-1 cells failed to prevent from ginsenoside Rh2-induced cell death. These results suggest the existence of other apoptotic pathway that requires induction of apoptosis by ginsenoside Rh2 rather than the pathway through Bcl-2, Bcl-x(L) or Bax in C6Bu-1 cells.