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Cerebrovascular Disease and Ischemia

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

The neuroprotective effects of a novel nucleoside analogue (2C1-C.OXT-A) on intracerebral hemorrhage

  • P3-330
  • 陸 豊 / Feng Lu:1 岡部 直彦 / Naohiko Okabe:1 氷見 直之 / Naoyuki Himi:1 中村-丸山 恵美 / Emi Nakamura-Maruyama:1 城本 高志 / Takashi Shiromoto:1 成田 和彦 / Kazuhiko Narita:1  塚本 郁子 / Ikuko Tsukamoto:2 丸山 徳見 / Tokumi Maruyama:3 榊原 紀和 / Norikazu Sakakibara:3 宮本 修 / Osamu Miyamoto:1 
  • 1:川崎医科大学 生理学2 / Physiology2, Kawasaki Medical School 2:香川大学医学部 薬物生体情報学 / Department of Pharmaco-Bio-Informatics, Faculty of Medicine, Kagawa University  3:徳島文理大学香川薬学部 薬物動態学 / Kagawa School of Phamaceutical Sciences,Tokushima Bunri University 

2Cl-C.OXT-A (COA-Cl) is a novel synthesized nucleoside analogue with the molecular weight of 284. It is soluble, stable and easy to synthesize. It has been reported that COA-Cl enhances angiogenesis in human umbilical endothelial cells (HUVEC). The previous study in our lab showed the neuroprotective effects of COA-Cl on ischemia stroke by reducing infarct volume and attenuating the behavioral deficits. The purpose of the present study is to evaluate the neuroprotective effect of COA-Cl on intracerebral hemorrhage (ICH), another common type of stroke, and investigate the potential mechanism of action. Sprague-Dawley (SD) rats were used for this study. ICH models were performed by the injection of 100μl autologous blood into the right basal ganglia. COA-Cl (30μg/kg) was injected intracerebroventricularly 10min after ICH. A battery of behavioral tests, including body swing test, forelimb placing test and corner turn test was performed to examine sensorimotor deficits with a time course as 1d, 3d, 5d and 7d after ICH. To understand the potential mechanism of how COA-Cl work at the acute phase of ICH, we examined brain edema 1day after ICH using water content test, and evaluated the anti-apoptosis role of COA-Cl by TUNEL assay. Oxidative stress, a primary cause for the edema formation, was also examined by a DNA oxidative marker (8-OHdG). Our results showed that the rats in COA-Cl group significantly attenuates the sensorimotor deficits and reduces brain edema compared with ICH ones. By immunohistochemistry method, we found that both TUNEL positive cells and 8-OHdG positive cells were fewer around the hematoma of COA-Cl treated rats compared with ICH ones. Theses results indicated that COA-Cl may have neuroprotective effects on ICH that it reduces brain edema, inhibits neuronal loss and improves ICH-induced behavioral deficits. Furthermore, we provide the first evidence that COA-Cl may have an anti-oxidative role, which may be one of the potential mechanisms for its neuroprotective effects.

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