The non-Antibiotic properties of Minocycline

Minocycline is a clinically available antibiotic and anti-inflammatory drug that because of its high lipid solubility has the capability to effectively cross the blood–brain barrier. Recent studies have focused on the anti-inflammatory, anti-apoptotic, and antioxidant properties of minocycline so its treatment provides neuroprotection against excitotoxic insults in a number of experimental models. The literature review was conducted using the electronic databases including Cochrane Library, Web of Science, Pubmed, Scopus and Google Scholar. The key words used as search terms were neuroprotective, CNS diseases, neurodegenerative diseases, neurotoxicity, poisoning, antibiotic since 2000 to 2018. Minocycline had been shown to provide protection in MPTP mouse model of Parkinson’s disease. Minocycline treatment improved the symptoms of ALS in mice via the inhibition of cytochrome c release and caspase activation. Minocycline suppresses T-cell proliferation, migration, and cytokine production in an autoimmune animal model of multiple sclerosis. Minocycline attenuates sevoflurane-induced cell injury by inhibiting apoptosis, reducing ROS production and blocking the activation of the NF-κB signaling pathway. Minocycline treatment significantly improved complexes I, IV, MPO and LDH activities, and also reduced the ADP/ATP ratio, lactate level, release of cytochrome c, and apoptosis in the kidney following aluminum phosphide poisoning, so it might be a possible candidate for the treatment of AlP-poisoning. Minocycline may ameliorate ethanol neurotoxicity in the developing by alleviating GSK3b-mediated neuro inflammation. The mechanism of minocycline in preventing Paraquat induced apoptosis might be mediated by attenuating endoplasmic reticulum stress and mitochondrial dysfunction, which respectively results in caspase-12 activation and the release of H2O2, HtrA2/Omi, and Smac/Diablo. Systemic administration of minocycline reduced intracerebral hemorrhage induced brain iron overload, brain injury and neurological deficits in that model. These effects may be linked to the role of minocycline as an iron chelator as well as an inhibitor of neuro inflammation Minocycline’s benefits lie in its ability to target multiple pathways mediating different aspects of apoptosis, inflammation and neuroprotective properties that are independent from its antimicrobial activity.