D-allose attenuates overexpression of inflammatory cytokines after cerebral ischemia/reperfusion injury in gerbil

著者

    • 篠原, 奈都代

書誌事項

タイトル

D-allose attenuates overexpression of inflammatory cytokines after cerebral ischemia/reperfusion injury in gerbil

著者名

篠原, 奈都代

学位授与大学

香川大学

取得学位

博士(医学)

学位授与番号

甲第643号

学位授与年月日

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.

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