Kim H E, Oh J H, Lee S K, Oh Y J
Department of Biology, Yonsei University College of Science, Seoul, Korea.
Life Sci. 1999;65(3):PL33-40. doi: 10.1016/s0024-3205(99)00252-0.
We used the rat C6 gliomal cell line to investigate the potential role of ginsenoside Rh2 (G-Rh2) in brain tumor. G-Rh2 induced many apoptotic manifestations in C6 gliomal cells as evidenced by changes in cell morphology, generation of DNA fragmentation, activation of caspase and production of reactive oxygen species (ROS). As a result, cotreatment with antioxidants or a broad-spectrum caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone effectively attenuated G-Rh2-induced cell death. However, specific cleavage of poly(ADP-ribose)polymerase into 85 kDa protein was not detected as demonstrated in many other apoptotic paradigms. Expression levels of Bcl-2 and Bax remained unchanged following G-Rh2 treatment. Furthermore, G-Rh2-induced cell death in C6 gliomal cells overexpressing antiapoptotic protein, Bcl-X(L), was comparable to that in parental cells. Taken together, our data indicate that G-Rh2-induced cell death is mediated by the generated ROS and the activation of caspase pathway in a Bcl-X(L)-independent manner.
我们使用大鼠C6胶质瘤细胞系来研究人参皂苷Rh2（G-Rh2）在脑肿瘤中的潜在作用。G-Rh2诱导C6胶质瘤细胞出现许多凋亡表现，细胞形态变化、DNA片段化产生、半胱天冬酶激活以及活性氧（ROS）生成均证明了这一点。结果，与抗氧化剂或广谱半胱天冬酶抑制剂N-苄氧羰基-Val-Ala-Asp-氟甲基酮共同处理可有效减轻G-Rh2诱导的细胞死亡。然而，在许多其他凋亡模式中所显示的聚（ADP-核糖）聚合酶特异性切割成85 kDa蛋白的情况未被检测到。G-Rh2处理后，Bcl-2和Bax的表达水平保持不变。此外，G-Rh2诱导过表达抗凋亡蛋白Bcl-X(L)的C6胶质瘤细胞死亡的情况与亲本细胞相当。综上所述，我们的数据表明，G-Rh2诱导的细胞死亡是以一种不依赖Bcl-X(L)的方式由产生的ROS和半胱天冬酶途径的激活介导的。
