Natsuyo Shinohara1, Takehiro Nakamura2, Yuko Abe1, Toru Hifumi1, Kenya Kawakita1, Aya Shinomiya3, Takashi Tamiya3, Masaaki Tokuda4, Richard F Keep5, Tohru Yamamoto6, Yasuhiro Kuroda1. 1. Emergency Medical Center, Kagawa University Hospital, Miki, Japan. 2. Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Takamatsu, Japan. Electronic address: tanakamu@kms.ac.jp. 3. Department of Neurological Surgery, Kagawa University Faculty of Medicine, Miki, Japan. 4. Department of Cell Physiology, Kagawa University Faculty of Medicine, Miki, Japan. 5. Department of Neurosurgery, University of Michigan, Ann Arbor, MI, USA. 6. Department of Molecular Neurobiology, Kagawa University Faculty of Medicine, Miki, Japan.
Abstract
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.
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.