Effectiveness of minocycline in acute white matter injury after intracerebral hemorrhage.
Zou X1, Wu Z1, Zhu W1, Chen L1, Mao Y1, Zhao F1.
J Neurosurg. 2016 Aug 5:1-8.
Abstract
OBJECTIVE Intracerebral hemorrhage (ICH) is a fatal disease with high morbidity and mortality, which may be followed by white matter injury (WMI) due to the local oxidizing reaction induced by iron (Fe). In this study, the authors examined the effect of
the tetracycline antibiotic minocycline on Fe-induced WMI and c-Jun N-terminal kinase (JNK) activation in rats. METHODS Thirty-six male Sprague-Dawley rats underwent an intracaudate injection of saline, Fe, or Fe + minocycline. Another 36 rats had an
intracaudate injection of autologous blood and were treated with minocycline or vehicle (saline). Biomarkers of both WMI and JNK activation were examined. RESULTS In the Fe-injection group, minocycline suppressed WMI labeled by β-amyloid precursor
protein (β-APP) and degraded myelin basic protein (dMBP)/MBP ratio. Protein levels of phosphorylated-JNK were increased after Fe injection, and could be suppressed by minocycline treatment. In the autologous blood-injection group, β-APP and dMBP/MBP
levels increased in the ipsilateral site compared with the contralateral site, which could be suppressed by 7 days of minocycline intervention. CONCLUSIONS Iron plays a critical role in WMI after ICH, which can be suppressed by minocycline through
reducing the damage induced by Fe.
KEYWORDS:
APP = amyloid precursor protein; Fe; GAPDH = glyceraldehyde 3-phosphate dehydrogenase; ICH = intracerebral hemorrhage; JNK = c-Jun N-terminal kinase; MBP = myelin basic protein; WMI = white matter injury; c-Jun N-terminal kinase; dMBP = degraded MBP;
intracerebral hemorrhage; iron; minocycline; vascular disorders; white matter injury
PMID: 27494818 DOI: 10.3171/2016.5.JNS152670
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