Nitric oxide-related toxicity in cultured astrocytes:: effect of Bacopa monniera

被引:69
作者
Russo, A
Borrelli, F
Campisi, A
Acquaviva, R
Raciti, G
Vanella, A
机构
[1] Univ Catania, Dept Biol Chem Med Chem & Mol Biol, I-95125 Catania, Italy
[2] Univ Naples, Dept Expt Pharmacol, I-80131 Naples, Italy
关键词
astrocytes; Bacopa monniera; DNA damage; nitric oxide; oxidants species;
D O I
10.1016/S0024-3205(03)00476-4
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
There is growing evidence that high concentrations of nitric oxide (NO), generated by activated astrocytes, might be involved in a variety of neurodegenerative diseases, such as Alzheimer's disease, ischemia and epilepsy. It has recently been suggested that glial cells may produce NO under superoxide radical stimulation by enzyme-independent mechanism. This suggests that also natural antioxidants may have therapeutical relevance in neurodegenerative diseases; Studies of Bhattacharya et al. have evidenced that Bacopa monniera (BM) (family Scrophulariaceae), an Ayurvedic medicinal plant clinically used for memory enhancing, epilepsy, insomnia and as a mild sedative, is able to reduce the memory-dysfunction in rat models of Alzheimer's disease, but the molecular mechanisms of this action are yet to be determined. In the present study, we examined the effect of a methanolic extract of BM on toxicity induced by the nitric oxide donor, S-nitroso-N-acetyl-penicillamine (SNAP), in culture of purified rat astrocytes. Our results indicate that, after 18 h of treatment, SNAP induced an increase in the production of reactive species, but did not induce the rupture of cellular membrane. Conversely, this NO donor induced a fragmentation of genomic DNA compared to control astrocytes. The extract of BM inhibited the formation of reactive species and DNA damage in a dose dependent manner. This data supports the traditional use of BM and indicates that this medicinal plant has a therapeutic potential in treatment or prevention of neurological diseases. (C) 2003 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:1517 / 1526
页数:10
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