The therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury

İsmailoğlu, Özgür; Atilla, Pergin; Palaoğlu, Selçuk; Çakar, Nur; Yaşar, Ümit; Kılınç, Kamer; Kaptanoğlu, Erkan

doi:10.5137/1019-5149.jtn.6197-12.1

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…Additionally, it also inhibits the pro-oxidative enzyme NO synthase upon stimulating glutathione peroxidase, SOD, and G-6-P dihydrogenase. Since melatonin is a lipophilic enzyme, it does not need a specific binding site or a receptor on the cell membrane (Ismailoglu et al 2012). Because acute oxidative stress is commonly involved in the progression of secondary neuronal tissue injury in these models, the neuroprotective effects of melatonin have been attributed by some authors to its activity as an antioxidant (Mesenge et al 1998, Cabrera et al 2000, Kaptanoglu et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Combination therapy with melatonin and dexamethasone in a mouse model of traumatic brain injury

Campolo¹,

Ahmad²,

Crupi³

et al. 2013

Journal of Endocrinology

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Traumatic brain injury (TBI) is a major cause of preventable death and morbidity in young adults. This complex condition is characterized by a significant blood-brain barrier leakage that stems from cerebral ischemia, inflammation, and redox imbalances in the traumatic penumbra of the injured brain. Recovery of function after TBI is partly through neuronal plasticity. In order to test whether combination therapy with melatonin and dexamethasone (DEX) might improve functional recovery, a controlled cortical impact (CCI) was performed in adult mice, acting as a model of TBI. Once trauma has occurred, combating these exacerbations is the keystone of an effective TBI therapy. The therapy with melatonin (10 mg/kg) and DEX (0.025 mg/kg) is able to reduce edema and brain infractions as evidenced by decreased 2,3,5-triphenyltetrazolium chloride staining across the brain sections. Melatoninand DEX-mediated improvements in tissue histology shown by the reduction in lesion size and an improvement in apoptosis level further support the efficacy of combination therapy. The combination therapy also blocked the infiltration of astrocytes and reduced CCI-mediated oxidative stress. In addition, we have also clearly demonstrated that the combination therapy significantly ameliorated neurological scores. Taken together, our results clearly indicate that combination therapy with melatonin and DEX presents beneficial synergistic effects, and we consider it an avenue for further development of novel combination therapeutic agents in the treatment of TBI that are more effective than a single effector molecule.

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Section: Introductionmentioning

confidence: 99%

Combination therapy with melatonin and dexamethasone in a mouse model of traumatic brain injury

Campolo¹,

Ahmad²,

Crupi³

et al. 2013

Journal of Endocrinology

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“…Ismailoglu et al [ 213 ] studied the therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury. These beneficial effects in rats after cerebral cortical injury seemed to be related to AOA of nimodipine.…”

Section: 14-dihydropyridines: a Separate Group Of Bioantioxidantsmentioning

confidence: 99%

1,4‐Dihydropyridine Derivatives: Dihydronicotinamide Analogues—Model Compounds Targeting Oxidative Stress

Velēna

Žarković

Trošelj

et al. 2016

Oxidative Medicine and Cellular Longevity

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Many 1,4-dihydropyridines (DHPs) possess redox properties. In this review DHPs are surveyed as protectors against oxidative stress (OS) and related disorders, considering the DHPs as specific group of potential antioxidants with bioprotective capacities. They have several peculiarities related to antioxidant activity (AOA). Several commercially available calcium antagonist, 1,4-DHP drugs, their metabolites, and calcium agonists were shown to express AOA. Synthesis, hydrogen donor properties, AOA, and methods and approaches used to reveal biological activities of various groups of 1,4-DHPs are presented. Examples of DHPs antioxidant activities and protective effects of DHPs against OS induced damage in low density lipoproteins (LDL), mitochondria, microsomes, isolated cells, and cell cultures are highlighted. Comparison of the AOA of different DHPs and other antioxidants is also given. According to the data presented, the DHPs might be considered as bellwether among synthetic compounds targeting OS and potential pharmacological model compounds targeting oxidative stress important for medicinal chemistry.

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Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat

Salman¹,

Kaushik²,

Tabassum

et al. 2020

Cell Mol Neurobiol

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The therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury

Abstract: Melatonin appears to have neuro-protective effects on the secondary brain damage while nimodipine and nimodipine plus melatonin combination did not show such neuro-protective effects on the secondary brain injury.

Cited by 4 publications

References 30 publications

Combination therapy with melatonin and dexamethasone in a mouse model of traumatic brain injury

Combination therapy with melatonin and dexamethasone in a mouse model of traumatic brain injury

1,4‐Dihydropyridine Derivatives: Dihydronicotinamide Analogues—Model Compounds Targeting Oxidative Stress

Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat

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