Protective effects of minocycline on experimental spinal cord injury in rats

Aras, Mustafa; Altaş, Murat; Motor, Sedat; Dokuyucu, Recep; Yılmaz, Atilla; Özgiray, Erkin; Seraslan, Yurdal; Yılmaz, Nebi

doi:10.1016/j.injury.2015.05.018

Cited by 27 publications

(16 citation statements)

References 30 publications

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“…Minocycline has also been reviewed recently for its effectiveness through multiple mechanisms for functional recovery from SCI [38]. The multiple targets that minocycline works for SCI functional recovery include upregulation of the protein VEGF and BDNF expressions; downregulation of protein p-38MAPK, proNGF, p75NTR, and RhoA expressions and suppressed caspase-3 activity [51]; and improved antioxidant activity through amelioration in oxidative stress in the SCI tissue [40].…”

Section: Discussionmentioning

confidence: 99%

“…Minocycline also eliminates free radicals in the post-SCI microenvironment and protects from oxidative stress [38]. It inhibits malondialdehyde, a by-product of lipid peroxidation [39,40], and increases glutathione (GSH) [39], superoxide dismutase, and glutathione peroxidase [40], suggesting the powerful antioxidative mechanisms of minocycline to recover from secondary injury in SCI. Minocycline is reported to inhibit matrix metalloproteinases (MMPs) that are upregulated following SCI and are involved in injury and recovery processes [41,42].…”

Section: Minocyclinementioning

confidence: 99%

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Effects of Cyclosporin-A, Minocycline, and Tacrolimus (FK506) on Enhanced Behavioral and Biochemical Recovery from Spinal Cord Injury in Rats

Ahmad¹,

Alshehri²

2019

Spinal Cord Injury Therapy [Working Title]

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Spinal cord injury (SCI) results into an immediate primary injury (physical damages) followed by secondary damages (prolonged posttraumatic inflammatory disorder) resulting into severe motor dysfunction including paralysis. The present chapter discusses and investigates the neuroprotective effects of cyclosporin-A (CsA), minocycline, and tacrolimus (FK506) and their therapeutic effectiveness in recovery from the animal model of SCI. Based on the available recent literature on these three drugs, as well as in perspective of the results obtained on some experimental behavioral, biochemical, and oxidative stress parameters in the present study, the therapeutical potential of these three drugs has been discussed. Furthermore, the animal model of SCI used herein has been reviewed and compared with other reported animal models for understanding the utility, suitability, and reproducibility of the methodology of the present model for screening purposes in quest of searching ideal therapeutic compounds for maximum recovery from SCI.

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Section: Discussionmentioning

confidence: 99%

Section: Minocyclinementioning

confidence: 99%

Effects of Cyclosporin-A, Minocycline, and Tacrolimus (FK506) on Enhanced Behavioral and Biochemical Recovery from Spinal Cord Injury in Rats

Ahmad¹,

Alshehri²

2019

Spinal Cord Injury Therapy [Working Title]

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“…Minocycline has antioxidant and antiapoptotic properties, probably acting at high doses as a direct radical scavenger, like vitamin E, due to its phenolic ring structure [40]. In rats with SCI, minocycline given at oral doses of 3, 30, and 90 mg/kg 1 and 24 h after the lesion reduced MDA concentration and increased GPx and SOD activity in a dose-dependent manner [41]. Minocycline decreased pro-inflammatory cytokines and the chemokines release from microglia and their activation, including their levels of enzymes that regulate LP and NO production [42].…”

Section: Minocyclinementioning

confidence: 99%

Current Developments in Antioxidant Therapies for Spinal Cord Injury

Villa¹,

Villamar²,

Zapien³

et al. 2019

Spinal Cord Injury Therapy [Working Title]

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When spinal cord injury (SCI) occurs, numerous sources of reactive oxygen species and nitrogen species may be active within first minutes or hours and even reactivate few days later. Free radical formation and lipid peroxidation (LP) have been described as an important mechanism in the beginning and accelerated progress in the development of diverse pathologies, importantly in those related to central nervous system. The compromise of molecules and cellular structures due to the oxidative state of microenvironment in SCI may determinate survival or apoptosis of resident and infiltrating cells and polarization toward an inflammatory response, which lead to an extension of damaged tissue and loss of neuronal function, or a regulatory/regenerative response. The investigation of new antioxidant agents and their action at a molecular level begins to reveal mechanisms that, if correctly modulated, promise an improvement in recovery of functions with respect to conventional pharmacological therapies. In this chapter, we will review the general mechanisms of oxidative stress and lipid peroxidation, those antioxidant treatments in experimental development and clinical phase, as well as their achievements and limitations.

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“…For example, the antibiotic minocycline was found to have neuroprotective effects and induce behavioral and cellular recovery after SCI in rats (Wells et al, 2003;Teng et al, 2004;Sonmez et al, 2013;Aras et al, 2015;Ahmad et al, 2016). The spectrum of effects of minocycline includes mitochondrial stabilization, inhibition of the release of cytochrome c, and antioxidant activity (Wells et al, 2003;Casha et al, 2012;Aras et al, 2015).…”

Section: Mitochondrial-based Treatmentmentioning

confidence: 99%

Mitochondrial-Based Therapeutics for the Treatment of Spinal Cord Injury: Mitochondrial Biogenesis as a Potential Pharmacological Target

Scholpa

Schnellmann

2017

J Pharmacol Exp Ther

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Spinal cord injury (SCI) is characterized by an initial trauma followed by a progressive cascade of damage referred to as secondary injury. A hallmark of secondary injury is vascular disruption leading to vasoconstriction and decreased oxygen delivery, which directly reduces the ability of mitochondria to maintain homeostasis and leads to loss of ATP-dependent cellular functions, calcium overload, excitotoxicity, and oxidative stress, further exacerbating injury. Restoration of mitochondria dysfunction during the acute phases of secondary injury after SCI represents a potentially effective therapeutic strategy. This review discusses the past and present pharmacological options for the treatment of SCI as well as current research on mitochondria-targeted approaches. Increased antioxidant activity, inhibition of the mitochondrial permeability transition, alternate energy sources, and manipulation of mitochondrial morphology are among the strategies under investigation. Unfortunately, many of these tactics address single aspects of mitochondrial dysfunction, ultimately proving largely ineffective. Therefore, this review also examines the unexplored therapeutic efficacy of pharmacological enhancement of mitochondrial biogenesis, which has the potential to more comprehensively improve mitochondrial function after SCI.

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Protective effects of minocycline on experimental spinal cord injury in rats

Cited by 27 publications

References 30 publications

Effects of Cyclosporin-A, Minocycline, and Tacrolimus (FK506) on Enhanced Behavioral and Biochemical Recovery from Spinal Cord Injury in Rats

Effects of Cyclosporin-A, Minocycline, and Tacrolimus (FK506) on Enhanced Behavioral and Biochemical Recovery from Spinal Cord Injury in Rats

Current Developments in Antioxidant Therapies for Spinal Cord Injury

Mitochondrial-Based Therapeutics for the Treatment of Spinal Cord Injury: Mitochondrial Biogenesis as a Potential Pharmacological Target

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