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线粒体靶向质体醌抗氧化剂 SkQR1 可降低大鼠创伤性神经功能缺损。

Mitochondria-targeted plastoquinone antioxidant SkQR1 decreases trauma-induced neurological deficit in rat.

机构信息

Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia.

出版信息

Biochemistry (Mosc). 2012 Sep;77(9):996-9. doi: 10.1134/S0006297912090052.

DOI:10.1134/S0006297912090052
PMID:23157258
Abstract

A protective effect of a mitochondria-targeted antioxidant, a cationic rhodamine derivative linked to a plastoquinone molecule (10-(6'-plastoquinonyl)decylrhodamine-19, SkQR1) was studied in the model of open focal trauma of rat brain sensorimotor cortex. It was found that daily intraperitoneal injections of SkQR1 (100 nmol/kg) for 4 days after the trauma improved performance in a test characterizing neurological deficit and decreased the volume of the damaged cortical area. Our results suggest that SkQR1 exhibits profound neuroprotective effect, which may be explained by its antioxidative activity.

摘要

一种靶向线粒体的抗氧化剂,一种连接到质体醌分子的阳离子罗丹明衍生物(10-(6'-质体醌基)癸基罗丹明-19,SkQR1)在大鼠大脑感觉运动皮层开放性局灶性创伤模型中进行了研究。结果发现,创伤后每天腹腔内注射 SkQR1(100nmol/kg)4 天,可改善神经功能缺损测试中的表现,并减少受损皮质区域的体积。我们的结果表明,SkQR1 表现出显著的神经保护作用,这可能与其抗氧化活性有关。

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