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Minocycline Attenuates Neonatal Germinal-Matrix-Hemorrhage-Induced Neuroinflammation and Brain Edema by Activating
Jun Tang1, Qianwei Chen1, Jing Guo1
1Department of Neurosurgery, Southwest Hospital, Third Military Medical University, No.30, Gaotanyan Street, Chongqing, 400038, People's Republic of China.
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.
Insights
Minocycline reduces brain injury and neuroinflammation in premature newborns with germinal matrix hemorrhage (GMH) by activating cannabinoid receptor 2 (CB2R). This suggests a potential therapeutic target for neonatal brain protection.
Area of Science:
- Neuroscience
- Neonatal Neurology
- Pharmacology
Background:
- Germinal matrix hemorrhage (GMH) is a leading cause of neurological deficits in premature infants.
- Cannabinoid receptor 2 (CB2R) is implicated in neurological inflammatory processes.
- Minocycline's neuroprotective effects in inflammatory conditions are partly mediated through CB2R.
Purpose of the Study:
- To investigate the efficacy of minocycline in reducing neuroinflammation and brain injury in a rat model of collagenase-induced GMH.
- To determine the role of CB2R activation in minocycline's neuroprotective effects.
Main Methods:
- A collagenase-induced GMH model was established in post-natal day 7 (P7) male rat pups.
- Minocycline, a CB2R antagonist (AM630), and a CB2R agonist (JWH133) were administered.
- Evaluated outcomes included CB2R expression, brain edema, microglial activation, lateral ventricular volume, and cortical thickness.
Main Results:
- Minocycline increased CB2R mRNA and protein expression in microglia.
- Minocycline significantly reduced GMH-induced brain edema, microglial activation, and lateral ventricular volume.
- Minocycline enhanced cortical thickness; these effects were abolished by AM630 and mimicked by JWH133.
Conclusions:
- Minocycline attenuates neuroinflammation and brain injury in a rat model of GMH.
- CB2R activation is partially involved in the neuroprotective mechanisms of minocycline in this model.
- Minocycline represents a potential therapeutic strategy for neonatal brain injury associated with GMH.
