NDLI: The Anti-inflammatory Effect of Melatonin on Methamphetamine-Induced Proinflammatory Mediators in Human Neuroblastoma Dopamine SH-SY5Y Cell Lines

Content Provider	Springer Nature Link
Author	Permpoonputtana, Kannika Govitrapong, Piyarat
Copyright Year	2012
Abstract	Methamphetamine (METH) is a highly addictive drug that is commonly abused worldwide. This psychostimulant drug causes the disturbances in the dopaminergic and serotonergic neurons of several brain areas. Exposure to METH has been shown to induce oxidative stress, reactive oxygen species, reactive nitrogen species, and neuroinflammation. However, the mechanism underlying METH-induced inflammation in neurons is still unclear. In this study, we investigated whether METH caused inflammatory effects in human dopaminergic neuroblastoma SH-SY5Y cells and whether this effect involved the nuclear factor-κB (NF-κB) transcription factor pathway. The present results showed that METH significantly increased inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner and significantly increased the levels of tumor necrosis factor (TNF)-α mRNA and phosphorylated NF-κB, which is translocated into the nucleus. Moreover, our results also show that METH downregulated another transcription factor, the nuclear factor erythroid 2-related factor (Nrf2), a transcription factor implicated in the expression of several antioxidant/detoxificant enzymes. Furthermore, we also examined the anti-inflammatory effect of melatonin against these METH-induced neuroinflammatory functions. The results show that melatonin significantly decreases the iNOS protein expression and TNF-α mRNA levels caused by METH. The activation and the level of pNF-κB were decreased while Nrf2 expression was increased when cells were pre-incubated with 100 nM of melatonin. In order to show the relationship between cell death and the increase of iNOS, 100 μM of l-NAME, an iNOS inhibitor pretreatment significantly prevented cell death caused by METH. These results demonstrate, for the first time, that METH directly induces inflammation in neurons via an NF-κB-dependent pathway and that the anti-neuroinflammatory effects of melatonin result from the inhibition of activated NF-κB in parallel with potentiated antioxidant/detoxificant defense by activated Nrf2 pathway.
Starting Page	189
Ending Page	199
Page Count	11
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	23
Issue Number	2
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2012-08-18
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Melatonin Proinflammatory Methamphetamine Tumor necrosis factor Inducible nitric oxide synthase Nuclear factor-κB Nuclear factor erythroid 2-related factor Neurosciences Neurology Neurochemistry Pharmacology/Toxicology Neurobiology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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