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Mediators of Inflammation
Volume 2010, Article ID 142458, 6 pages
Clinical Study

Elevation of High-Mobility Group Protein Box-1 in Serum Correlates with Severity of Acute Intracerebral Hemorrhage

1Department of Neurology, Daping Hospital, The Third Military Medical University, Changjiang Branch Road no. 10, Yuzhong District, Chongqing 400042, China
2Department of Radiology, Daping Hospital, The Third Military Medical University, Yuzhong District, Chongqing 400042, China
3College of Biomedical Engineering, Chongqing University, Chongqing 400044, China
4Department of Neurosurgery, Daping Hospital, The Third Military Medical University, Yuzhong District, Chongqing 400042, China

Received 9 August 2010; Accepted 7 September 2010

Academic Editor: Steven Kunkel

Copyright © 2010 Yu Zhou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


High-mobility group protein box-1 (HMGB1) is a proinflammatory involved in many inflammatory diseases. However, its roles in intracerebral hemorrhage (ICH) remain unknown. The purpose of this study was to examine the correlation between changes in serum levels of HMGB1 following acute ICH and the severity of stroke as well as the underlying mechanism. Changes in serum levels of HMGB1 in 60 consecutive patients with primary hemispheric ICH within 12 hours of onset of symptoms were determined. The correlation of HMGB1 with disease severity, IL-6, and TNF- was analyzed. Changes in HMGB1 levels were detected with ELISA and Western blot. Compared with normal controls, patients with ICH had markedly elevated levels of HMGB1, which was significantly correlated with the levels of IL-6 and TNF- , NIHSS score at the 10th day, and mRS score at 3 months. In comparison with the control group, the levels of HMGB1 in the perihematomal tissue in mice with ICH increased dramatically, peaked at 72 hours, and decreased at 5 days. Meanwhile, heme could stimulate cultured microglia to release large amounts of HMGB1 whereas ions failed to stimulate HMGB1 production from microglia. Our findings suggest that HMGB1 may play an essential role in the ICH-caused inflammatory injury.