Hydroxysafflor yellow A inhibits rat brain mitochondrial permeability transition pores by a free radical scavenging action

被引:65
作者
Tian, Jingwei [1 ]
Li, Guisheng [1 ]
Liu, Zhifeng [1 ]
Fu, Fenghua [1 ]
机构
[1] Yantai Univ, Sch Pharm, Yantai 264003, Shandong, Peoples R China
关键词
hydroxysafflor yellow A; mitochondrial permeability transition pore; reactive oxygen species; neuroprotection;
D O I
10.1159/000141653
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Hydroxysafflor yellow A (HSYA), the major and most active antioxidant from Carthamus tinctorius L., has been clinically prescribed in China to treat patients with cerebral ischemia, but the detailed mechanism is not known. This study examines the effect of HSYA on mitochondrial permeability transition pores (mtPTP) in the rat brain. HSYA at 10-80 mu mol (.) l(-1) inhibited Ca2+- and H2O2-induced swelling of mitochondria isolated from rat brains. The addition of Ca2+ generated reactive oxygen species (ROS) in isolated mitochondria. HSYA (10-80 mu mol (.) l(-1)) inhibited Ca2+-induced generation of ROS. At the same time, HSYA significantly improved mitochondrial energy metabolism, enhanced ATP levels and the respiratory control ratio. These results suggest that HSYA inhibits the opening of mtPTP by a free radical scavenging action in the brain, and this may contribute to the neuroprotective effect of HSYA. Copyright (C) 2008 S. Karger AG, Basel.
引用
收藏
页码:121 / 126
页数:6
相关论文
共 19 条
[1]   A mitochondrial perspective on cell death [J].
Bernardi, P ;
Petronilli, V ;
Di Lisa, F ;
Forte, M .
TRENDS IN BIOCHEMICAL SCIENCES, 2001, 26 (02) :112-117
[2]   Mitochondrial intermembrane junctional complexes and their role in cell death [J].
Crompton, M .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 529 (01) :11-21
[3]   Inhibition of glutamate release via recovery of ATP levels accounts for a neuroprotective effect of aspirin in rat cortical neurons exposed to oxygen-glucose deprivation [J].
De Cristóbal, J ;
Cárdenas, A ;
Lizasoain, I ;
Leza, JC ;
Fernández-Tomé, P ;
Lorenzo, P ;
Moro, MA .
STROKE, 2002, 33 (01) :261-267
[4]   T-817MA, a novel neurotrophic agent, improves sodium nitroprusside-induced mitochondrial dysfunction in cortical neurons [J].
Fukushima, T ;
Koide, M ;
Ago, Y ;
Baba, A ;
Matsuda, T .
NEUROCHEMISTRY INTERNATIONAL, 2006, 48 (02) :124-130
[5]   The permeability transition pore complex: another view [J].
Halestrap, AP ;
McStay, GP ;
Clarke, SJ .
BIOCHIMIE, 2002, 84 (2-3) :153-166
[6]  
Kinter DB, 1997, J NEUROCHEM, V69, P1219
[7]   Mitochondrial control of cell death [J].
Kroemer, G ;
Reed, JC .
NATURE MEDICINE, 2000, 6 (05) :513-519
[8]  
Liu F, 1992, Yao Xue Xue Bao, V27, P785
[9]   Protective effect of serotonin on 6-hydroxydopamine- and dopamine-induced oxidative damage of brain mitochondria and synaptosomes and PC12 cells [J].
Park, JW ;
Youn, YC ;
Kwon, OS ;
Jang, YY ;
Han, ES ;
Lee, CS .
NEUROCHEMISTRY INTERNATIONAL, 2002, 40 (03) :223-233
[10]   The mitochondrial permeability transition mediates both necrotic and apoptotic death of hepatocytes exposed to Br-A23187 [J].
Qian, T ;
Herman, B ;
Lemasters, JJ .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1999, 154 (02) :117-125