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Mol Neurobiol. 2016 Apr;53(3):1935-1948. doi: 10.1007/s12035-015-9154-x. Epub 2015 Apr 2.

Minocycline Attenuates Neonatal Germinal-Matrix-Hemorrhage-Induced Neuroinflammation and Brain Edema by Activating Cannabinoid Receptor 2.

Author information

1
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, No.30, Gaotanyan Street, Chongqing, 400038, People's Republic of China.
2
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, No.30, Gaotanyan Street, Chongqing, 400038, People's Republic of China. zhichen@tmmu.edu.cn.
3
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, No.30, Gaotanyan Street, Chongqing, 400038, People's Republic of China. gangzhu6666@sina.com.

Abstract

Germinal matrix hemorrhage (GMH) is the most common neurological disease of premature newborns leading to detrimental neurological sequelae. Minocycline has been reported to play a key role in neurological inflammatory diseases by controlling some mechanisms that involve cannabinoid receptor 2 (CB2R). The current study investigated whether minocycline reduces neuroinflammation and protects the brain from injury in a rat model of collagenase-induced GMH by regulating CB2R activity. To test this hypothesis, the effects of minocycline and a CB2R antagonist (AM630) were evaluated in male rat pups that were post-natal day 7 (P7) after GMH. We found that minocycline can lead to increased CB2R mRNA expression and protein expression in microglia. Minocycline significantly reduced GMH-induced brain edema, microglial activation, and lateral ventricular volume. Additionally, minocycline enhanced cortical thickness after injury. All of these neuroprotective effects of minocycline were prevented by AM630. A cannabinoid CB2 agonist (JWH133) was used to strengthen the hypothesis, which showed the identical neuroprotective effects of minocycline. Our study demonstrates, for the first time, that minocycline attenuates neuroinflammation and brain injury in a rat model of GMH, and activation of CBR2 was partially involved in these processes.

KEYWORDS:

Cannabinoid receptor 2; Germinal matrix hemorrhage; Microglia; Minocycline; Neuroinflammation

PMID:
25833102
DOI:
10.1007/s12035-015-9154-x
[Indexed for MEDLINE]

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