Melatonin attenuates methamphetamine‐induced overexpression of pro‐inflammatory cytokines in microglial cell lines

Tocharus, Jiraporn; Khonthun, Chakkrapong; Chongthammakun, Sukumal; Govitrapong, Piyarat

doi:10.1111/j.1600-079x.2010.00761.x

Cited by 91 publications

(72 citation statements)

References 49 publications

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“…Melatonin at 1 nM, which approximates the physiological concentration of the pineal hormone at night, significantly inhibited TNF-a, IL-1b, IL-6, and iNOS overexpression induced by methamphetamine (METH) in microglia (184). In addition, the antiinflammatory effect of melatonin against these METHinduced neuroinflammatory events also occurs in human neuroblastoma dopaminergic cells (185).…”

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confidence: 82%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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Abstract. Neural aging as a progressive loss of function involves central and peripheral postmitotic neurons and neural stem cells (NSCs). It promotes neurodegeneration, impairs neurogenesis, and can be considered a cause of cognitive impairment and sensory and motor deficits in the elderly. Age-related morphological atrophic changes and cellular alterations are addressed by neural aging mechanisms. Neurogenesis declines during aging through several mechanisms such as an increase in quiescence state, changes in lineage fate, telomerase dysfunction, the failure of the DNA repair system, increased apoptosis, and the impairment of self-renewal. The selfrenewal transcriptional factor Sox2 has been correlated with retrotransposon L1 and certain cellcycle-and epigenetic-related factors, which are sometimes considered age-related factors in NSC aging. As neurogenesis decreases, non-mitotic neurons undergo neurodegeneration by oxidative stress, sirtuin, insulin signaling and mTOR alteration, mitochondrial dysfunction, and protein misfolding and aggregation. As neurodegeneration and impaired neurogenesis promote the nervous system aging process, the identification of neuronal anti-aging is required to raise life expectancy. The role of melatonin in increasing neurogenesis and protecting against neurodegeneration has been investigated. Here, we review nervous system aging that is correlated with mechanisms of neurodegeneration and the impairment of neurogenesis and evaluate the effects of melatonin on these processes.

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confidence: 82%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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“…Recent studies have demonstrated that METH is a neurotoxic drug that can induce neuronal (Ajjimaporn et al, 2005;Zhu et al, 2006;Deng et al, 2007) and glial cell death by several pathways, including oxidative stress (Riddle et al, 2006;Tocharus et al, 2008), mitochondrial dysfunction (Brown et al, 2005;Jumnongprakhon et al, 2014), excitotoxicity (Staszewski and Yamamoto, 2006;Ernst and Chang, 2008), inflammatory responses (Jumnongprakhon et al, 2015), and ER stress (Shah and Kumar, 2016). We have previously reported that exposure to METH causes an overproduction of ROS (Tocharus et al, 2010) that leads to oxidative stress. METH also induces cell death mediated by the apoptosis pathway through the mitochondrial death pathway (Imam et al, 2001;Thiriet et al, 2001;Jumnongprakhon et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…The physiological functions of melatonin include circadian maintenance, sleep promotion, and immune enhancement (Nelson and Drazen, 2000;Zisapel, 2001;Pandi-Perumal et al, 2008;Tan et al, 2009;Manchester et al, 2015). Our previous studies suggested that melatonin is a neuroprotective agent that can down-regulate the expression of not only reactive oxygen species (ROS) and nitric oxide (NO) but also pro-inflammatory cytokines (Tocharus et al, 2008(Tocharus et al, , 2010. Moreover, melatonin also attenuates METH-induced glial cell death by decreasing the inflammatory responses and the mitochondrial death pathway (Jumnongprakhon et al, 2014(Jumnongprakhon et al, , 2015.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have suggested that METH is a neurotoxic drug that can cause pathological changes and death in neuronal and glial cells (Thompson et al, 2004;Kitamura et al, 2007Kitamura et al, , 2010Takeichi et al, 2012). METH induces glial cell hyperactivity and death via many pathways, including apoptosis, oxidative stress, inflammation, interruption of mitochondrial function, and endoplasmic reticulum (ER)-stress responses (Tocharus et al, 2010;Jumnongprakhon et al, 2014Jumnongprakhon et al, , 2015Shah and Kumar, 2016). METH also induces neuronal apoptosis in the striatal neurons of mice by disturbing the function of the ER, leading to ER stress (Riddle et al, 2006;Deng et al, 2007;Jayanthi et al, 2014;Wongpayoon and Govitrapong, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Melatonin suppresses methamphetamine-triggered endoplasmic reticulum stress in C6 cells glioma cell lines

et al. 2017

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-Methamphetamine (METH) is a neurotoxic drug that causes brain damage by inducing neuronal and glial cell death together with glial cell hyperactivity-mediated progressive neurodegeneration. Previous studies have shown that METH induced glial cell hyperactivity and death via oxidative stress, the inflammatory response, and endoplasmic reticulum stress (ER stress) mechanisms, and melatonin could reverse these effects. However, the exact mechanism of the protective role of melatonin in METH-mediated ER stress has not been understood. This study investigated the protective effect of melatonin against METH toxicity-mediated ER stress in glial cells. Our study demonstrated that METH increased glial cell toxicity related to METH-induced ER stress by stimulating the unfolded protein response (UPR) to activate the expression of ER stress transducers, including phosphorylated doublestranded RNA-activated protein kinase (PKR)-like ER kinase (p-PERK), activating transcription factor (ATF6), and phosphorylated inositol-requiring enzyme 1 (p-IRE1). Moreover, the expression of binding immunoglobulin protein (Bip), CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, phosphorylated eukaryotic translation initiation factor 2 alpha (p-eIF2α) and spliced X-box-binding protein-1 (XBP-1) mRNA were also increased. Melatonin reduced ER stress induced by METH toxicity by reducing the expression of ER stress response genes and proteins in a concentration-dependent manner. In addition, melatonin promoted the expression of Bip chaperone in a concentration-dependent manner. Taken together, our findings suggest that melatonin can protect against ER stress-induced glial cell death induced by METH.

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“…The administration of METH induces toxicity in both neuronal and glial cells, mediated by an increase in reactive oxygen species (ROS) [3][4][5][6] and pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin (IL)-6, IL1b, and nitric oxide (NO) both in vitro [7][8][9][10] and in vivo [11][12][13] that play important roles in the pathogenesis of neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease [14][15][16][17]. Recently, it has become widely accepted that the response of the microglial cells or astrocyte cells to METH is associated with the pathogenesis of diseases [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Protects Methamphetamine-Induced Neuroinflammation Through NF-κB and Nrf2 Pathways in Glioma Cell Line

et al. 2015

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Methamphetamine (METH) is known as a toxin for neuronal and glial cells. Previous studies have found that METH-induced glial cell death and inflammation is mediated by oxidative stress. However, the exact mechanisms of the inflammatory response remain unclear. Therefore, we hypothesized that the activation of nuclear factor-κB (NF-κB) signaling, a key mediator of inflammation, and the inhibition of nuclear factor erythroid 2-related factor-2 (Nrf2) signaling, a regulator of the antioxidant response, would be significant events occurring in response to METH-induced inflammation in a rat glioma cell line (C6 cells). Our results show that METH increased the production of nitric oxide (NO) and up-regulated the expression of its main regulatory protein, inducible nitric oxide synthase (iNOS). METH also induced NF-κB activation by increasing inhibitory κBα (IκBα) degradation and translocation of the NF-κB (p65) subunit into the nucleus. Additionally, METH inhibited the activation of the Nrf2 pathway by decreasing the translocation of Nrf2 into the nucleus and also by suppressing the expression of heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase-1 (NQO-1), and glutamate-cysteine ligase catalytic subunit (γ-GCLC), resulting in the suppression of superoxide dismutase (SOD) activity. Pretreatment with melatonin effectively promoted Nrf2 activation and reversed the METH-induced NF-κB response. Melatonin increased the expression of HO-1, NQO-1, and γ-GCLC, resulting in increased SOD activity. In addition, melatonin also decreased IκBα degradation, translocation of the p65 subunit, and expression of iNOS, resulting in decreased NO production. Taken together, our results indicate that melatonin diminishes the proinflammatory mediator in METH-stimulated C6 cells by inhibiting NF-κB activation and inducing Nrf2-mediated HO-1, NQO-1, and γ-GCLC expression.

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Melatonin attenuates methamphetamine‐induced overexpression of pro‐inflammatory cytokines in microglial cell lines

Cited by 91 publications

References 49 publications

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

Melatonin suppresses methamphetamine-triggered endoplasmic reticulum stress in C6 cells glioma cell lines

Melatonin Protects Methamphetamine-Induced Neuroinflammation Through NF-κB and Nrf2 Pathways in Glioma Cell Line

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