Minocycline

Early modulation of pro-inflammatory microglia by minocycline loaded nanoparticles confers long lasting protection after spinal cord injury.

Model: Contusive spinal cord injury

Acute treatment with minocycline loaded nanoparticles modulated resident microglia, reduced the pro-inflammatory response and maintained a pro-regenerative environment, improving behavioural outcome up to 63 days post injury. The approach also demonstrated a mechanistic link between early microglia…

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Anti-inflammatory treatments during the chronic phase of spinal cord injury improve locomotor function in adult mice.

Model: T9 contusion spinal cord injury

Minocycline or anti-CD25 antibody given during the chronic phase improved hindlimb locomotor function after spinal cord injury in mice.

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Selective nanovector mediated treatment of activated proinflammatory microglia/macrophages in spinal cord injury

Model: Experimental spinal cord injury in a mouse model, with in vitro and in vivo assessment of the subacute phase of secondary injury

Minocycline loaded nanoparticles reduced activation and proliferation of microglia and macrophages around the lesion site, shifted cells from a round phagocytic-like phenotype towards an arborised resting-like phenotype with low CD68 staining, and reduced proinflammatory IL-6 expression with persis…

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Hyperphosphorylated neurofilament NF-H as a biomarker of the efficacy of minocycline therapy for spinal cord injury.

Model: Acute spinal cord contusion

Minocycline reduced plasma pNF-H levels, which correlated with better hind limb motor recovery after SCI.

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Minocycline restores olfactory bulb volume and olfactory behavior after traumatic brain injury in mice.

Model: Closed-head injury by mechanical percussion

Minocycline attenuated olfactory behavioural deficit and olfactory bulb atrophy up to 12 weeks after traumatic brain injury.

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Minocycline restores sAPPalpha levels and reduces the late histopathological consequences of traumatic brain injury in mice.

Model: Weight-drop traumatic brain injury

Minocycline attenuated the post-TBI decrease in sAPPalpha and reduced long-term brain atrophy and gliosis.

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Minocycline neuroprotection in a rat model of asphyxial cardiac arrest is limited.

Model: Asphyxial cardiac arrest (5 min) followed by resuscitation

Minocycline transiently reduced neuronal degeneration and microglial response at 7 days (most effective given post-arrest) but the neuroprotection was lost by 21 days.

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Co-delivery of minocycline and paclitaxel from injectable hydrogel for treatment of spinal cord injury.

Model: Spinal cord hemisection

Dual-drug treatment reduced inflammation at 7 days, decreased scar tissue and increased neuronal regeneration at 28 days, and produced faster and sustained functional improvement compared with the other experimental groups.

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Effectiveness of minocycline and FK506 alone and in combination on enhanced behavioral and biochemical recovery from spinal cord injury in rats.

Model: Experimental spinal cord injury by weight compression method

Both drugs produced significant behavioural recovery, supported by histopathological, monoamine and oxidative stress findings, with the ranking FK506 plus minocycline greater than minocycline greater than FK506 across all parameters.

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Minocycline Transiently Reduces Microglia/Macrophage Activation but Exacerbates Cognitive Deficits Following Repetitive Traumatic Brain Injury in the Neonatal Rat.

Model: Repetitive impact traumatic brain injury modelling abusive head trauma, three impacts delivered 24 h apart in 11-day-old rats

Minocycline reduced microglial and macrophage reactivity in the corpus callosum at 3 days but not 7 days post-injury, had no effect on axonal injury, neurodegeneration or tissue atrophy, and exacerbated injury-induced spatial memory deficits.

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Prevention of hypoglycemia-induced neuronal death by minocycline.

Model: Insulin-induced severe acute hypoglycaemia under isoflurane anaesthesia and controlled ventilation: 10 U/kg regular insulin intraperitoneally, hypoglycaemia terminated after 30 min of isoelectric EEG by 0.2 mL of 50% glucose intravenously followed by continuous 1:1 50% glucose and Krebs-Henseleit infusion at 1.5 mL/h for 3 h; achieved blood glucose 0.40 plus or minus 0.03 mM (vehicle) and 0.38 plus or minus 0.01 mM (minocycline); mean arterial pressure maintained 120 to 180 mmHg; sham animals received the same insulin dose but were kept normoglycaemic with 25% glucose

Minocycline started 6 h after glucose reperfusion reduced hippocampal and cortical microglial activation and myeloperoxidase immunoreactivity, significantly increased surviving CA1 NeuN-positive neurons at 7 days and 8 weeks with fewer Fluoro-Jade B positive cells, and prevented hypoglycaemia-induc…

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Analysis of minocycline as a countermeasure against acute radiation syndrome.

Model: Whole-body irradiation with 1-3 Gy cobalt-60 gamma rays

Minocycline increased splenic macrophages, granulocytes, natural killer, T and CD8+ T cells, raised IL-1alpha, IL-1beta, GM-CSF and G-CSF, and suppressed MIP-1alpha, TNF-alpha and interferon-gamma compared with radiation alone.

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Evaluation of late cognitive impairment and anxiety states following traumatic brain injury in mice: the effect of minocycline.

Model: Closed-head traumatic brain injury by mechanical percussion under anaesthesia

Closed-head injury produced a recognition memory deficit persisting to at least 13 weeks with no clear change in anxiety; minocycline attenuated the memory impairment in an effective and lasting manner.

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Minocycline improves functional outcomes, memory deficits, and histopathology after endovascular perforation-induced subarachnoid hemorrhage in rats.

Model: Endovascular perforation-induced subarachnoid haemorrhage

High-dose minocycline reduced brain water content and MMP-9 activity at 24 h, improved spatial memory and attenuated hippocampal and cortical neuronal loss; low-dose minocycline did not reduce brain oedema.

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Osteopontin expression in acute immune response mediates hippocampal synaptogenesis and adaptive outcome following cortical brain injury.

Model: Unilateral entorhinal cortex lesion producing hippocampal deafferentation and reactive synaptogenesis

Osteopontin protein and transcript rose more than 50-fold in activated glia at 1 to 2 days after lesion. Minocycline attenuated MMP-9 activity, reduced LCN2 expression and osteopontin fragment generation, and attenuated removal of synapsin-1 positive axons from the deafferented zone. Osteopontin kn…

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Melatonin and minocycline for combinatorial therapy to improve functional and histopathological deficits following traumatic brain injury

Model: Controlled cortical impact (1.5 mm) traumatic brain injury

Neither melatonin, minocycline nor their combination significantly improved cognitive or histological outcomes after TBI.

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Blockade of acute microglial activation by minocycline promotes neuroprotection and reduces locomotor hyperactivity after closed head injury in mice: a twelve-week follow-up study

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Minocycline alleviates death of oligodendrocytes by inhibiting pro-nerve growth factor production in microglia after spinal cord injury

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Minocycline inhibits contusion-triggered mitochondrial cytochrome c release and mitigates functional deficits after spinal cord injury

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Neuroprotection by minocycline facilitates significant recovery from spinal cord injury in mice

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Differential implication of proinflammatory cytokine interleukin-6 in the development of cephalic versus extracephalic neuropathic pain in rats

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