Carnitine-induced senescence in glioblastoma cells.
Carnitine-induced senescence in glioblastoma cells.
复制标题
肉碱诱导胶质母细胞瘤细胞衰老。
DOI：
10.3892/etm.2012.556
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发表时间：
2012
影响因子：
2.7
通讯作者：
M. Yoshikawa
中科院分区：
文献类型：
--
作者：
S. Yamada;R. Matsuda;F. Nishimura;I. Nakagawa;Y. Motoyama;Young;Mitsutoshi Nakamura;H. Nakase;Y. Ouji;M. Yoshikawa
肉毒碱是细胞中脂质代谢所必需的，并且已知具有抗氧化特性。以前的研究表明抗氧化剂能够诱导胶质母细胞瘤细胞衰老，因此，在本研究中，我们研究了肉毒碱对胶质母细胞瘤细胞的影响。在低营养条件下，胶质母细胞瘤细胞的增殖减弱，细胞内肉毒碱水平增加。胶质母细胞瘤细胞增殖在补充有外源性肉毒碱的培养物中也减弱，其中通过衰老相关β-gal（SA-β-gal）染色检测衰老的诱导。然而，没有证据表明诱导细胞凋亡。当细胞与肉毒碱加p38丝裂原活化蛋白激酶（MAPK）抑制剂培养时，未检测到这些作用。因此，肉毒碱似乎在正常细胞中具有抗氧化作用，但在胶质母细胞瘤细胞中诱导衰老，这可能被视为相反的现象。据报道，暴露于替莫唑胺的细胞会衰老，替莫唑胺是一种用于治疗胶质母细胞瘤的标准药物。因此，肉毒碱可能是胶质母细胞瘤的一种有吸引力的替代疗法。
Carnitine is essential for lipid metabolism in cells and is known to possess antioxidant properties. Previous reports have suggested that antioxidants are able to induce senescence in glioblastoma cells, consequently, in the present study, we investigated the effect of carnitine on glioblastoma cells. Under conditions of hyponutrition (undernutrition), the proliferation of glioblastoma cells was attenuated and the level of intracellular carnitine was increased. Glioblastoma cell proliferation was also attenuated in cultures that were supplemented with exogenous carnitine, where the induction of senescence was detected by senescence-associated β-gal (SA-β-gal) staining. However, there was no evidence of the induction of apoptosis. These effects were not detected when cells were cultured with carnitine plus an inhibitor of p38 mitogen-activated protein kinase (MAPK). It, therefore, appears that carnitine has antioxidant actions in normal cells but induces senescence, which may be regarded as an opposite phenomenon, in glioblastoma cells. Senescence has been reported in cells exposed to temozolomide, which is a standard drug used for the treatment of glioblastoma. Carnitine could, therefore, represent an attractive alternative therapy for glioblastoma.
DOI：
10.1152/ajpheart.2000.279.5.h2124
发表时间：
2000-11-01
影响因子：
4.8
作者：
Sparagna, GC;Hickson-Bick, DL;McMillin, JB
通讯作者：
McMillin, JB