Therapeutic window for cinnamophilin following oxygen-glucose deprivation and transient focal cerebral ischemia

被引:33
|
作者
Lee, E-Jian [1 ]
Chen, Hung-Yi [1 ,2 ]
HungA, Yu-Chang [1 ]
Chen, Tsung-Ying [1 ,3 ,4 ]
Lee, Ming-Yang [1 ]
Yu, Shu-Ching [1 ]
Chen, Ying-Hsin [1 ]
Chuang, I-Chuan [1 ,5 ]
Wu, Tian-Shung [6 ]
机构
[1] Natl Cheng Kung Univ, Med Ctr & Med Sch, Dept Surg, Neurosurg Serv,Neurophysiol Lab, Tainan 70428, Taiwan
[2] China Med Univ, Inst Pharm, Taichung, Taiwan
[3] Buddhist Tzu Chi Univ, Dept Anesthesiol, Hualien, Taiwan
[4] Buddhist Tzu Chi Gen Hosp, Hualien, Taiwan
[5] Chia Nan Univ Pharm & Sci, Dept Biotechnol, Tainan, Taiwan
[6] Natl Cheng Kung Univ, Dept Chem, Tainan 70428, Taiwan
关键词
Acute stroke; Lipid peroxidation assay; Radical scavenging assay; Neuroinflammation; Therapeutic window of opportunity; Cinnamophilin; THROMBOXANE A(2) RECEPTOR; REDUCES OXIDATIVE DAMAGE; BRAIN INFARCT VOLUME; SPRAGUE-DAWLEY RATS; ARTERY OCCLUSION; DELAYED TREATMENT; ENERGY DEPLETION; FREE-RADICALS; STROKE; REPERFUSION;
D O I
10.1016/j.expneurol.2009.01.019
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cinnamophilin (CINN, (8R, 8'S)-4, 4'-dihydroxy-3, 3'-dimethoxy-7-oxo-8, 8'-neolignan) protects against ischemic stroke in mice. While some anti-oxidative effects of CINN have been characterized, its therapeutic window and molecular basis for neuroprotection remain unclear. We evaluated antioxidant and anti-inflammatory properties and therapeutic window of CINN against brain ischemia using a panel of in vitro and in vivo assays. Data from lipid peroxidation and radical scavenging assays showed that CINN was a robust antioxidant and radical scavenger. CINN effectively inhibited the production of tumor necrosis factor alpha (TNF-alpha), nitrite/nitrate, interleukin-6 (IL-6) in lipopolysaccharide (LPS)-stimulated RAW 264.7 and BV2 cells (P<0.05, respectively). Relative to controls, CINN, administrated at 80 mg/kg, 2, 4, or 6 h postinsult, but not 12 h, significantly reduced brain infarction by 34-43% (P<0.05) and improved neurobehavioral outcome (P<0.05) following transient focal cerebral ischemia in rats. CINN (10-30 mu M) also significantly reduced oxygen-glucose deprivation-induced neuronal damage (P<0.05) in rat organotypic hippocampal slices, even when it was administrated 2, 4, or 6 h postinsult. Together, CINN protects against ischemic brain damage with a therapeutic window up to 6 h in vivo and in vitro, which may, at least in part, be attributed by its direct antioxidant and anti-inflammatory effects. (C) 2009 Elsevier Inc, All rights reserved.
引用
收藏
页码:74 / 83
页数:10
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