WITHDRAWN: Melatonin improves methamphetamine-induced blood brain barrier impairment through NADPH oxidase-2 in primary rat brain microvascular endothelium cells

Jumnongprakhon, Pichaya; Govitrapong, Piyarat; Tocharus, Chainarong; Tocharus, Jiraporn

doi:10.1016/j.brainres.2016.06.014

Cited by 4 publications

(2 citation statements)

References 73 publications

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“…Previous studies showed that treatment of melatonin could exert an anti-inflammatory effect via inhibiting the TLR4/NF-κB signaling pathway in several disease models [ 55 , 56 ]. Besides, melatonin promotes the BBB integrity in methamphetamine-induced inflammation in primary rat brain microvascular ECs [ 57 ]. However, the underlying signaling pathway in neonatal HII is still not fully studied.…”

Section: Discussionmentioning

confidence: 99%

Melatonin protects against blood-brain barrier damage by inhibiting the TLR4/ NF-κB signaling pathway after LPS treatment in neonatal rats

Wang

Pan

et al. 2017

Oncotarget

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Hypoxic-ischemic and inflammatory (HII) induces the disruption of blood–brain barrier (BBB) which leads to inflammatory responses and neuronal cell death, resulting in brain secondary damage. Previous studies showed that melatonin produced potent neuroprotective effects in neonatal hypoxic-ischaemic models. However, the relationship between BBB disruption and melatonin in HII was still unclear. The present study therefore investigated the beneficial effects of melatonin on BBB after HII and the underlying mechanisms. HII animal model was conducted by receiving lipopolysaccharide followed by 90 min hypoxia-ischaemia in postnatal day 2 Sprague–Dawley rat pups. Melatonin was injected intraperitoneally 1 h before lipopolysaccharide injection and then once a day for 1 week to evaluate the long-term effects. In this study, we demonstrated that melatonin administration inhibited the disruption of BBB permeability and improved the white matter recovery in HII model rats. Melatonin significantly attenuated the degradation of junction proteins and the neuroprotective role was related to the inhibition of microglial toll-like receptor 4/ nuclear factor-kappa B signaling pathway both in vivo and in vitro. Taken together, our data demonstrated that therapeutic strategies targeting inflammation might be suitable for the therapy of preserving BBB integrity after HII.

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Section: Discussionmentioning

confidence: 99%

Melatonin protects against blood-brain barrier damage by inhibiting the TLR4/ NF-κB signaling pathway after LPS treatment in neonatal rats

Wang

Pan

et al. 2017

Oncotarget

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“…Induction of Nrf2 has also been associated with the effects of melatonin in reducing oxidative and nitrosative DNA damage [ 312 ]. In fact, numerous investigations have shown that melatonin activates phase-2 antioxidative enzymes, via the Nrf2 pathway, including heme oxygenase-1 (HO-1), γ-glutamylcysteine synthetase (γ-GSC), nicotinamide adenine dinucleotide phosphate (NADPH): quinone dehydrogenase-1 (NQO1) and SOD [ 313 , 314 , 315 , 316 , 317 , 318 , 319 , 320 , 321 , 322 , 323 , 324 , 325 , 326 , 327 , 328 , 329 , 330 , 331 , 332 , 333 ].…”

Section: Antioxidant Protectionmentioning

confidence: 99%

Melatonin: A Versatile Protector against Oxidative DNA Damage

2018

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Oxidative damage to DNA has important implications for human health and has been identified as a key factor in the onset and development of numerous diseases. Thus, it is evident that preventing DNA from oxidative damage is crucial for humans and for any living organism. Melatonin is an astonishingly versatile molecule in this context. It can offer both direct and indirect protection against a wide variety of damaging agents and through multiple pathways, which may (or may not) take place simultaneously. They include direct antioxidative protection, which is mediated by melatonin’s free radical scavenging activity, and also indirect ways of action. The latter include, at least: (i) inhibition of metal-induced DNA damage; (ii) protection against non-radical triggers of oxidative DNA damage; (iii) continuous protection after being metabolized; (iv) activation of antioxidative enzymes; (v) inhibition of pro-oxidative enzymes; and (vi) boosting of the DNA repair machinery. The rather unique capability of melatonin to exhibit multiple neutralizing actions against diverse threatening factors, together with its low toxicity and its ability to cross biological barriers, are all significant to its efficiency for preventing oxidative damage to DNA.

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Melatonin charge transfer complex with 2,3-dichloro-5,6-dicyano-1,4-benzoquinone: Molecular structure, DFT studies, thermal analyses, evaluation of biological activity and utility for determination of melatonin in pure and dosage forms

Mohamed

Hamed

Zaki

et al. 2017

Spectrochimica Acta Part A: Molecular and Biomolecular Spectros

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WITHDRAWN: Melatonin improves methamphetamine-induced blood brain barrier impairment through NADPH oxidase-2 in primary rat brain microvascular endothelium cells

Cited by 4 publications

References 73 publications

Melatonin protects against blood-brain barrier damage by inhibiting the TLR4/ NF-κB signaling pathway after LPS treatment in neonatal rats

Melatonin protects against blood-brain barrier damage by inhibiting the TLR4/ NF-κB signaling pathway after LPS treatment in neonatal rats

Melatonin: A Versatile Protector against Oxidative DNA Damage

Melatonin charge transfer complex with 2,3-dichloro-5,6-dicyano-1,4-benzoquinone: Molecular structure, DFT studies, thermal analyses, evaluation of biological activity and utility for determination of melatonin in pure and dosage forms

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