D-allose attenuates overexpression of inflammatory cytokines after cerebral ischemia/reperfusion injury in gerbil
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著者
書誌事項
- タイトル
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D-allose attenuates overexpression of inflammatory cytokines after cerebral ischemia/reperfusion injury in gerbil
- 著者名
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篠原, 奈都代
- 学位授与大学
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香川大学
- 取得学位
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博士(医学)
- 学位授与番号
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甲第643号
- 学位授与年月日
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2016-06-28
注記・抄録
BackgroundThe present study investigates the effects of d-allose, a rare sugar, on the inflammatory response after transient forebrain ischemia in the gerbil and whether it reduces oxidative stress (8-hydroxyl-2′-deoxyguanosine levels) and behavioral deficits.
MethodsTransient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 minutes. d-Allose was intraperitoneally injected immediately after ischemia (400 mg/kg). Inflammatory cytokines and oxidative damage in the hippocampus and behavioral deficits were examined 3 days after ischemia.
Resultsd-Allose administration reduced ischemia-induced cytokine production, oxidative stress, and behavioral deficits (motor and memory related).
ConclusionsThe present results suggest that d-allose reduces brain injury after transient global ischemia by suppressing inflammation as well as by inhibiting oxidative stress.
Background The present study investigates the effects of d-allose, a rare sugar, on the inflammatory response after transient forebrain ischemia in the gerbil and whether it reduces oxidative stress (8-hydroxyl-2′-deoxyguanosine levels) and behavioral deficits.
Methods Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 minutes. d-Allose was intraperitoneally injected immediately after ischemia (400 mg/kg). Inflammatory cytokines and oxidative damage in the hippocampus and behavioral deficits were examined 3 days after ischemia.
Results d-Allose administration reduced ischemia-induced cytokine production, oxidative stress, and behavioral deficits (motor and memory related).
Conclusions The present results suggest that d-allose reduces brain injury after transient global ischemia by suppressing inflammation as well as by inhibiting oxidative stress.