Celastrol causes apoptosis and cell cycle arrest in rat glioma cells

被引：71

作者：

Ge, Pengfei ^{[1
]}

Ji, Xunming ^{[2
]}

Ding, Yuchuan ^{[3
]}

Wang, Xiaofei ^{[4
]}

Fu, Shuangliin ^{[1
]}

Meng, Fankai ^{[1
]}

Jin, Xin ^{[1
]}

Ling, Feng ^{[2
]}

Luo, Yinan ^{[1
]}

机构：

[1] Jilin Univ, Dept Neurosurg, Hosp 1, Changchun 130021, Peoples R China

[2] Capital Univ Med Sci, Xuanwu Hosp, Dept Neurosurg, Beijing 10053, Peoples R China

[3] Wayne State Univ, Sch Med, Dept Neurosurg, Detroit, MI 48201 USA

[4] Nihon Univ, Dept Adv Med Sci, Div Canc Genet, Sch Med, Tokyo 1028251, Japan

来源：

NEUROLOGICAL RESEARCH | 2010年 / 32卷 / 01期

关键词：

Celastrol; apoptosis; cell cycle; proteasome; glioma; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PROTEASOME INHIBITOR; CANCER; DEGRADATION; TRIPTERINE; INDUCTION; GROWTH;

D O I：

10.1179/016164109X12518779082273

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

100204 [神经病学];

摘要：

Glioma still remains a major health problem in the world. Celastrol has been proved to be an effective natural proteasome inhibitor and was used for treatment of autoimmune disease, chronic inflammation and neurodegenerative disease. However, its effect on glioma is unclear. In this study, we investigated the therapeutic effects of celastrol on C6 glioma cells. The results demonstrated that celastrol inhibited cell proliferation in a time-and dose-dependent manner, suppressed proteasome chymotrypsin-like activity and induced apoptosis and cell cycle arrest at G2/M phase in C6 cells. Proapoptosis proteins bax and caspase-3 were up-regulated, as well as cell cycle G2/M-related proteins cyclin B-1, p21 and p27. Conversely, anti-apoptosis proteins bcl-2 and XIAP and cell cycle regulator cyclin-dependent kinase 2 were down-regulated. Taken together, our data suggest that celastrol can suppress proteasome activity and induce apoptosis and cell cycle arrest in C6 glioma cells, which make it be a potential drug for glioma.

引用

页码：94 / 100

页数：7

共 30 条

[1]

Celastrol, a potent antioxidant and anti-inflammatory drug, as a possible treatment for Alzheimer's disease [J].