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Hemeoxygenase-1 in SJL mice with experimental allergic encephalomyelitis

Department of Molecular and Integrative Physiology, Mental Retardation and Human Development Center, University of Kansas Medical Center, Kansas City, KS 66160

M R Emerson

Department of Molecular and Integrative Physiology, Mental Retardation and Human Development Center, University of Kansas Medical Center, Kansas City, KS 66160

S M LeVine

Department of Molecular and Integrative Physiology, Mental Retardation and Human Development Center, University of Kansas Medical Center, Kansas City, KS 66160, slevine{at}kumc.edu

The expression of heme oxygenase-1 (HO -1) is increased in the C NS of mice and rats with experimental allergic encephalo myelitis (EAE), an animal model of multiple sclerosis (MS). To investigate the role of HO -1 in EAE, a putative inhibitor [tin-pro toporphyrin IX (Sn-PP IX)] of HO -1 was administered to SJL mice during active disease. Sn-PP IX (200 mmol/kg) attenuated clinical scores, weight loss, and some signs of patho logy in comparison to vehicle treatment. G lutathione levels were greater in treated EAE mice than in those receiving vehicle, indicating lower oxidative stress in the former group. These data suggest that inhibition of HO -1 attenuated disease and suppressed free radical production. In the SJL model of EAE, extravasated blood is present in the C NS, and iron released by HO -1 from this heme source may not be adequately sequestered by ferritin, allowing for iron-mediated tissue damage. Thus, HO -1 may act to amplify the disease process in this model.

Key Words: experimental allergic encephalomyelitis • ferritin • heme oxygenase-1 • iron • multiple sclerosis • oxidative stress • tin-protoporphyrin IX

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