Neuroprotective Effects of Astaxanthin in Oxygen-Glucose Deprivation in SH-SY5Y Cells and Global Cerebral Ischemia in Rat

被引:80
作者
Lee, Dae-Hee [2 ,3 ]
Lee, Yong J. [2 ,3 ]
Kwon, Ki Han [1 ]
机构
[1] Gwangju Univ, Coll Hlth Welf & Educ, Dept Food Sci & Nutr, Kwangju 503703, South Korea
[2] Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA 15213 USA
[3] Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15213 USA
关键词
astaxanthin; global ischemia; oxidative stress; neuroprotection; nitric oxide synthase; heat shock protein; NITRIC-OXIDE SYNTHASE; GENE-EXPRESSION; BRAIN-INJURY; CAROTENOIDS; DAMAGE; HYPERTHERMIA; PROTECTION; TOXICITY; EXTRACT; MODEL;
D O I
10.3164/jcbn.10-29
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Astaxanthin (ATX), a naturally occurring carotenoid pigment, is a powerful biological antioxidant. In the present study, we investigated whether ATX pharmacologically offers neuroprotection against oxidative stress by cerebral ischemia. We found that the neuroprotective efficacy of ATX at the dose of 30 mg/kg (n = 8) was 59.5% compared with the control group (n = 3). In order to make clear the mechanism of ATX neuroprotection, the up-regulation inducible nitric oxide synthase (iNOS) and heat shock proteins (HSPs) together with the oxygen glucose deprivation (OGD) in SH-SY5Y cells were also investigated. The induction of various factors involved in oxidative stress processes such as iNOS was suppressed by the treatment of ATX at 25 and 50 mu M after OGD-induced oxidative stress. In addition, Western blots showed that ATX elevated of heme oxygenase-1 (HO-1; Hsp32) and Hsp70 protein levels in in vitro. These results suggest that the neuroprotective effects of ATX were related to anti-oxidant activities in global ischemia.
引用
收藏
页码:121 / 129
页数:9
相关论文
共 33 条
[1]   BIOLOGICAL ACTIONS OF CAROTENOIDS [J].
BENDICH, A ;
OLSON, JA .
FASEB JOURNAL, 1989, 3 (08) :1927-1932
[2]  
Britton G., 1995, Carotenoids, V1
[3]   EFFECT OF MILD HYPERTHERMIA ON THE ISCHEMIC INFARCT VOLUME AFTER MIDDLE CEREBRAL-ARTERY OCCLUSION IN THE RAT [J].
CHEN, H ;
CHOPP, M ;
WELCH, KMA .
NEUROLOGY, 1991, 41 (07) :1133-1135
[4]   TRANSIENT HYPERTHERMIA PROTECTS AGAINST SUBSEQUENT FOREBRAIN ISCHEMIC CELL-DAMAGE IN THE RAT [J].
CHOPP, M ;
CHEN, H ;
HO, KL ;
DERESKI, MO ;
BROWN, E ;
HETZEL, FW ;
WELCH, KMA .
NEUROLOGY, 1989, 39 (10) :1396-1398
[5]   LY178002 REDUCES RAT-BRAIN DAMAGE AFTER TRANSIENT GLOBAL FOREBRAIN ISCHEMIA [J].
CLEMENS, JA ;
HO, PPK ;
PANETTA, JA .
STROKE, 1991, 22 (08) :1048-1052
[6]   Effects of tempol, a membrane-permeable radical scavenger, in a gerbil model of brain injury [J].
Cuzzocrea, S ;
McDonald, MC ;
Mazzon, E ;
Siriwardena, D ;
Costantino, G ;
Fulia, F ;
Cucinotta, G ;
Gitto, E ;
Cordaro, S ;
Barberi, I ;
De Sarro, A ;
Caputi, AP ;
Thiemermann, C .
BRAIN RESEARCH, 2000, 875 (1-2) :96-106
[7]   Down-regulation of neuronal nitric oxide synthase by nitric oxide after oxygen-glucose deprivation in rat forebrain slices [J].
De Alba, J ;
Cárdenas, A ;
Moro, MA ;
Leza, JC ;
Lorenzo, P ;
Boscá, L ;
Lizasoain, I .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (01) :248-254
[8]   Characterization of LY231617 protection against hydrogen peroxide toxicity [J].
Fuson, KS ;
Mark, RJ ;
Panetta, JA ;
May, PC .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (03) :1154-1160
[9]   Many mechanisms for Hsp70 protection from cerebral ischemia [J].
Giffard, RG ;
Yenari, MA .
JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY, 2004, 16 (01) :53-61
[10]  
Giugliano D, 2000, NUTR METAB CARDIOVAS, V10, P38