Heme oxygenase-1 in SJL mice with experimental allergic encephalomyelitis

被引：52

作者：

Chakrabarty, A ^{[1
]}

Emerson, MR ^{[1
]}

LeVine, SM ^{[1
]}

机构：

[1] Univ Kansas, Med Ctr, Dept Mol & Integrat Physiol, Mental Retardat & Human Dev Ctr, Kansas City, KS 66160 USA

来源：

MULTIPLE SCLEROSIS | 2003年 / 9卷 / 04期

关键词：

experimental allergic encephalomyelitis; ferritin; heme oxygenase-1; iron; multiple sclerosis; oxidative stress; tin-protoporphyrin IX;

D O I：

10.1191/1352458503ms928oa

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The expression of heme oxygenase-1 (HO-1) is increased in the CNS 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-protoporphyrin IX (Sn-PP IX)] of HO-1 was administered to SJL mice during active disease. Sn-PP IX ( 200 mumol/kg) attenuated clinical scores, weight loss, and some signs of pathology in comparison to vehicle treatment. Glutathione 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 CNS, 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 pro cess in this model.

引用

页码：372 / 381

页数：10

共 53 条

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