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Minocycline targets multiple secondary injury mechanisms in traumatic spinal cord injury
Journal article   Open access   Peer reviewed

Minocycline targets multiple secondary injury mechanisms in traumatic spinal cord injury

Robert B Shultz and Yinghui Zhong
Neural regeneration research, v 12(5), pp 702-713
May 2017
PMID: 28616020
url
https://doi.org/10.4103/1673-5374.206633View
Published, Version of Record (VoR)CC BY-NC-SA V4.0 Open

Abstract

glutamate exitotoxicity inflammation minocycline neuroprotection calcium influx P38 MAPK anti-oxidant cytochrome c oxidative stress PI3K/Akt
Minocycline hydrochloride (MH), a semi-synthetic tetracycline derivative, is a clinically available antibiotic and anti-inflammatory drug that also exhibits potent neuroprotective activities. It has been shown to target multiple secondary injury mechanisms in spinal cord injury, its anti-inflammatory, anti-oxidant, and anti-apoptotic properties. The secondary injury mechanisms that MH can potentially target include inflammation, free radicals and oxidative stress, glutamate excitotoxicity, calcium influx, mitochondrial dysfunction, ischemia, hemorrhage, and edema. This review discusses the potential mechanisms of the multifaceted actions of MH. Its anti-inflammatory and neuroprotective effects are partially achieved through conserved mechanisms such as modulation of p38 mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt signaling pathways as well as inhibition of matrix metalloproteinases (MMPs). Additionally, MH can directly inhibit calcium influx through the N-methyl-D-aspartate (NMDA) receptors, mitochondrial calcium uptake, poly(ADP-ribose) polymerase-1 (PARP-1) enzymatic activity, and iron toxicity. It can also directly scavenge free radicals. Because it can target many secondary injury mechanisms, MH treatment holds great promise for reducing tissue damage and promoting functional recovery following spinal cord injury.

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Web of Science research areas
Cell Biology
Neurosciences
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