Evaluation of the anti-angiogenic action of melatonin in breast cancer

Jardim, Bruna Victorasso; Ferreira, Lívia Carvalho; Borin, Thaiz F.; Moschetta, Marina Gobbe; Gelaleti, Gabriela Bottaro; Lopes, Jair; Maschio, Larissa Bazela; Leonel, Camila; Gonçalves, Naiane N; Martins, Gustavo Rodrigues; Zuccari, Débora A.P.C.

doi:10.1186/1753-6561-7-s2-p11

Cited by 6 publications

(3 citation statements)

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“…MLT serves as an immune enhancer, anti-inflammatory agent [43], free-radical scavenger [44], human mood-and behavior-modulating agent [45], and anticancer agent [46,47]. It is also involved in the oral cavity [48], traumatic CNS injury [2], an anti-angiogenic molecule in breast tumors [49], and sleep regulation [50]. MLT activity is mainly regulated and governed by MT1 and MT2, which are widely distributed in CNS and primarily found in suprachiasmatic nuclei in the hypothalamus of the mammalian cells.…”

Section: Synthesis Biology and Functions Of Mltmentioning

confidence: 99%

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

Gurunathan

Kang

Kim

2020

Cancers

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Melatonin (MLT) is a powerful chronobiotic hormone that controls a multitude of circadian rhythms at several levels and, in recent times, has garnered considerable attention both from academia and industry. In several studies, MLT has been discussed as a potent neuroprotectant, anti-apoptotic, anti-inflammatory, and antioxidative agent with no serious undesired side effects. These characteristics raise hopes that it could be used in humans for central nervous system (CNS)-related disorders. MLT is mainly secreted in the mammalian pineal gland during the dark phase, and it is associated with circadian rhythms. However, the production of MLT is not only restricted to the pineal gland; it also occurs in the retina, Harderian glands, gut, ovary, testes, bone marrow, and lens. Although most studies are limited to investigating the role of MLT in the CNS and related disorders, we explored a considerable amount of the existing literature. The objectives of this comprehensive review were to evaluate the impact of MLT on the CNS from the published literature, specifically to address the biological functions and potential mechanism of action of MLT in the CNS. We document the effectiveness of MLT in various animal models of brain injury and its curative effects in humans. Furthermore, this review discusses the synthesis, biology, function, and role of MLT in brain damage, and as a neuroprotective, antioxidative, anti-inflammatory, and anticancer agent through a collection of experimental evidence. Finally, it focuses on the effect of MLT on several neurological diseases, particularly CNS-related injuries.

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Section: Synthesis Biology and Functions Of Mltmentioning

confidence: 99%

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

Gurunathan

Kang

Kim

2020

Cancers

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“…The rate of endogenous melatonin synthesis depends on the action of its precursors, the amino acid as well as a neurotransmitter serotonin, arylalkylamine N-acetyltransferase, (AANAT) and tryptophan hydroxylase (TPH) in a circadian and seasonal manner [ 40 ] ( Figure 1 ). There are a number of studies where melatonin has been shown to regulate various physiological functions in the body such as immune enhancing, anti-inflammatory properties [ 43 ], radicals scavenger [ 44 ], traumatic CNS injury [ 4 ], modulation of human mood and behaviour [ 45 ], anticancer activity [ 46 , 47 ], in oral cavity [ 48 ], against angiogenesis in breast tumors [ 49 ], sleep regulation [ 50 ].…”

Section: Biology Of Melatoninmentioning

confidence: 99%

Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

Naseem

Parvez

2014

The Scientific World Journal

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Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS). Traumatic brain injury (TBI) is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κ β, disruption of blood-brain barrier (BBB), and oxidative stress. Spinal cord injury (SCI) includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.

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“…Melatonin is an ideal neuroprotective agent as it readily crosses the blood-brain barrier and lacks toxicity in comparison to other neuro-protectants [15]. There is evidence supporting the role of melatonin in regulation of various physiological functions like modulation of sleep, mood, behavior, anti-inflammatory activities, radical scavenging, immunomodulatory activities, antiangiogenic activity, and anti-carcinogenic properties, and so forth [16][17][18][19][20]. Melatonin receptors are widely distributed in central nervous system (CNS), as well as in the peripheral organs which acts as a lipophilic and hydrophilic molecule and able to pass the morpho-physiological barriers such as the blood-brain barrier (BBB) [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Neuronal apoptosis can be prevented by the combined therapy with melatonin and hypothermia in a neonatal rat model of hypoxic-ischemic encephalopathy

Toader

Hoteiuc

Bidian

et al. 2021

Medicine and Pharmacy Reports

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Introduction. Birth hypoxia is a leading cause of perinatal mortality and neurological morbidity, resulting in central nervous system injury. Cerebral hypoxia and ischemia can produce a severe brain damage following a typical pattern, defined by selective vulnerability of the brain regions. The neonates are most prone to hypoxic-ischemic injuries due to the lack of efficient antioxidant defense. Neonatal hypoxia–ischemia (HI) in a 7-day-old rat HI model can produce cell death by apoptotic or necrotic mechanisms. The degree of apoptotic or necrotic mechanisms responsible for cell death in neonatal hypoxia–ischemia are not very clear as yet. The form of neuronal death may also depend on the severity of ischemic injury. Necrosis predominates in more severe cases, whereas apoptosis occurs in areas with milder ischemic injury. A human study demonstrated apoptotic and necrotic forms of cell death after hypoxic injury, whereas in some brains from stillbirths, only apoptotic figures were observed. The expression of activated caspase-3 reflects the role of apoptosis in neonatal hypoxic ischemic brain injury. Objectives. The aim of this study was to evaluate the possible neuroprotective effect of melatonin and hypothermia in hypoxic-ischemic encephalopathy in newborn rats. Local damages induced by hypoxia and ischemia were assessed by evaluating the changes in terms of histology and apoptosis. Methods. The experiment was conducted on 20 newborn Wistar rats premedicated for seven days with melatonin in a dose of 20 mg/kg/day. On the 7th postnatal day (P7), the newborn rats were exposed to ischemia (by clamping the right carotid artery) and hypobaric hypoxia (8% O2 for 90 minutes) and some groups to hypothermia. Results. In this experimental model of neonatal encephalopathy, melatonin, in a dose of 20 mg/kg/day has neuroprotective effect by reducing the number of cells expressing apoptosis in Cornu Ammonis (CA) (Ammon’s Horn) CA1, CA2, CA3 and dentate gyrus of the hippocampus when combined with hypothermia. Conclusion. The results of this study prove that melatonin is protective in ischemic-hypoxic brain injuries, but the protection is conditioned in most of the brain regions (excepting cerebral cortex) by conjugation with post-injury hypothermia treatment.

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Evaluation of the anti-angiogenic action of melatonin in breast cancer

Cited by 6 publications

References 0 publications

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers

Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

Neuronal apoptosis can be prevented by the combined therapy with melatonin and hypothermia in a neonatal rat model of hypoxic-ischemic encephalopathy

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