Anti-Inflammatory and Antioxidant Actions of &lt;b&gt;&lt;i&gt;N&lt;/i&gt;&lt;/b&gt;-Arachidonoyl Serotonin in RAW264.7 Cells

Jeon, Hye Lyun; Yoo, Jae Myung; Lee, Bo Dam; Lee, Su Jin; Sohn, Eun Jung; Kim, Mee Ree

doi:10.1159/000443739

Cited by 18 publications

(17 citation statements)

References 35 publications

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“…Lipid peroxidation was determined following a method reported previously [22]. Briefly, brains isolated from sacrificed mice were homogenized in ice-cold 1× PBS, and then the homogenates were centrifuged (17,000× g at 4 • C) for 10 min.…”

Section: Determination Of Lipid Peroxidationmentioning

confidence: 99%

3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

et al. 2019

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3,3′-Diindolylmethane (DIM), a metabolite of indole-3-carbinol present in Brassicaceae vegetables, possesses various health-promoting effects. Nonetheless, the effect of DIM on neurodegenerative diseases has not been elucidated clearly. In this study, we hypothesized DIM may protect neuronal cells against oxidative stress-induced apoptosis by promoting the formation of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes through stabilizing the activation of the tropomyosin-related kinase receptor B (TrkB) cascade and we investigated the effect of DIM on oxidative stress-mediated neurodegenerative models. DIM protected neuronal cells against oxidative stress-induced apoptosis by regulating the expression of apoptosis-related proteins in glutamate-treated HT-22 cells. Additionally, DIM improved the expression of BDNF and antioxidant enzymes, such as heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and NAD(P)H quinine oxidoreductase-1, by promoting the activation of the TrkB/protein kinase B (Akt) pathway in the cells. Consistent with in vitro studies, DIM attenuated memory impairment by protecting hippocampal neuronal cells against oxidative damage in scopolamine-treated mice. Conclusionally, DIM exerted neuroprotective and antioxidant actions through the activation of both BDNF production and antioxidant enzyme formation in accordance with the TrkB/Akt pathway in neuronal cells. Such an effect of DIM may provide information for the application of DIM in the prevention of and therapy for neurodegenerative diseases.

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Section: Determination Of Lipid Peroxidationmentioning

confidence: 99%

3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

et al. 2019

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“…There are three major known pathways of melatonin degradation: (a) the classical hepatic catabolic pathway that generates 6-hydroxymelatonin that is then excreted via the kidney as a sulphate conjugate [ 3 , 5 , 25 , 26 ]; (b) the alternative indolic pathway that produces 5-methoxyindole acetic acid or 5-methoxytryptophol [ 27 , 28 ]; and (c) the kynuric pathway that produces N 1 -acetyl-N 2 -formyl-5-kynuramine (AFMK) [ 29 – 31 ]. In addition to the antioxidant properties of melatonin, AFMK and N 1 -acetyl-5-methoxykinuramine (AMK) are two important melatonin metabolites that have excellent radical scavenging activity [ 5 , 32 , 33 ].…”

Section: Melatoninmentioning

confidence: 99%

“…In general, melatonin is highly effective in protecting cells from damage under severe inflammatory conditions [ 32 , 45 , 53 , 115 , 116 ]. There are several sites where melatonin may interfere during the inflammatory process.…”

Section: Melatonin and Inflammationmentioning

confidence: 99%

Melatonin as an Anti-Inflammatory Agent Modulating Inflammasome Activation

Favero

Franceschetti

Bonomini

et al. 2017

International Journal of Endocrinology

188

128

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Inflammation may be defined as the innate response to harmful stimuli such as pathogens, injury, and metabolic stress; its ultimate function is to restore the physiological homeostatic state. The exact aetiology leading to the development of inflammation is not known, but a combination of genetic, epigenetic, and environmental factors seems to play an important role in the pathogenesis of many inflammation-related clinical conditions. Recent studies suggest that the pathogenesis of different inflammatory diseases also involves the inflammasomes, intracellular multiprotein complexes that mediate activation of inflammatory caspases thereby inducing the secretion of proinflammatory cytokines. Melatonin, an endogenous indoleamine, is considered an important multitasking molecule with fundamental clinical applications. It is involved in mood modulation, sexual behavior, vasomotor control, and immunomodulation and influences energy metabolism; moreover, it acts as an oncostatic and antiaging molecule. Melatonin is an important antioxidant and also a widespread anti-inflammatory molecule, modulating both pro- and anti-inflammatory cytokines in different pathophysiological conditions. This review, first, gives an overview concerning the growing importance of melatonin in the inflammatory-mediated pathological conditions and, then, focuses on its roles and its protective effects against the activation of the inflammasomes and, in particular, of the NLRP3 inflammasome.

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“…N ‐Arachidonoyl serotonin, one of endocannabinoids, is known to inactivate transient receptor potential vanilloid1 channel, a Ca 2+ ion channel, and inhibit fatty acid amide hydrolase . In addition, N ‐arachidonoyl serotonin has been found to possess some beneficial effects such as antioxidant, anti‐allergy, and anti‐inflammation . Previously, we found that N ‐palmitoyl serotonin (Pal‐5HT) possessed more potent neuroprotective activity than other N ‐acyl serotonins in preventing neuronal cells against oxidative stress‐induced cytotoxicity .…”

Section: Introductionmentioning

confidence: 99%

Anti‐Apoptotic Effect of N‐Palmitoyl Serotonin on Glutamate‐Mediated Apoptosis Through Secretion of BDNF and Activation of TrkB/CREB Pathway in HT‐22 Cells

Yoo

Lee

et al. 2017

Euro J Lipid Sci & Tech

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Recently, N‐acyl serotonins have been reported to exert neuroprotective actions against oxidative stress by inducing antioxidant enzymes. However, the mechanisms for the neuroprotective action of N‐acyl serotonins are still not clarified. In this study, we focuse on the suppressive effect of N‐palmitoyl serotonin on glutamate‐induced apoptosis in HT‐22 cells, and then examine the molecular mechanism for anti‐apoptotic action of N‐palmitoyl serotonin. For this purpose, flow cytometry, immunoblotting analysis and antibody‐mediated neutralization is formed. When HT‐22 cells are preincubated with N‐palmitoyl serotonin prior to glutamate treatment, N‐palmitoyl serotonin dose‐dependently reduces apoptotic bodies, and recoveres mitochondrial potential in glutamate‐treated HT‐22 cells. Further, N‐palmitoyl serotonin concentration‐dependently increases the expression of B‐cell lymphoma 2 (Bcl‐2), an anti‐apoptotic factor, whereas it reduces the expression of Bcl‐2‐associated X protein, apoptosis‐inducing factor, Ca2+‐dependent non‐lysosomal cysteine protease, cytochrome c, and cleaves caspase‐3. Meanwhile, N‐palmitoyl serotonin enhanced phosphorylation of tropomyosin‐related kinase receptors (TrkB) and cAMP response element‐binding protein (CREB) as well as expression of brain‐derived neurotrophic factor (BDNF). Separately, the inclusion of anti‐BDNF antibody neutralizes the neuroprotective action of N‐palmitoyl serotonin against glutamate‐induced cell death. In addition, K252a, a TrkB inhibitor, also reverses neuroprotective effect of N‐palmitoyl serotonin, suggesting that the action of N‐palmitoyl serotonin may be expressed through the formation of BDNF. Based on these results, it is proposed that N‐palmitoyl serotonin promotes formation and secretion of BDNF, and then protects neuronal cells against oxidative stress‐induced apoptosis through activation of TrkB/CREB pathway. Practical Applications: The results may provide further information for the application of N‐acyl serotonins as a therapeutic or preventive agent for neurodegenerative diseases. N‐Palmitoyl 2 serotonin (Pal‐5HT) not only induces brain‐derived neurotrophic factor (BDNF) expression but also protects neuronal cells against oxidative stress.

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Anti-Inflammatory and Antioxidant Actions of <b><i>N</i></b>-Arachidonoyl Serotonin in RAW264.7 Cells

Cited by 18 publications

References 35 publications

3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

Melatonin as an Anti-Inflammatory Agent Modulating Inflammasome Activation

Anti‐Apoptotic Effect of N‐Palmitoyl Serotonin on Glutamate‐Mediated Apoptosis Through Secretion of BDNF and Activation of TrkB/CREB Pathway in HT‐22 Cells

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