Anti-Inflammatory and Anti-Oxidative Effects of AM404 in IL-1β-Stimulated SK-N-SH Neuroblastoma Cells

Apweiler, Matthias; Streyczek, Jana; Saliba, Soraya Wilke; Ditrich, Johannes; Muñóz, Eduardo; Fiebich, Bernd L.

doi:10.3389/fphar.2021.789074

Cited by 7 publications

(6 citation statements)

References 53 publications

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“…The inhibition of oxidative stress/isoprostane pathways independent of COX-2 might be responsible for the reduction of PGE 2 by KIT C and KIT H as well, as discussed in our previous study [42] showing that COX enzymatic activity is enhanced by antioxidative stress [43]. In this and a previous study, KIT C as well as KIT H decreased oxidative stress and 8-Iso-PGF 2α synthesis via GPR55 coupled to the inhibition of PGE 2 and therefore possibly affecting the AA pathway by reduced COX-activity [17].…”

Section: Discussionsupporting

confidence: 53%

Functional Selectivity of Coumarin Derivates Acting via GPR55 in Neuroinflammation

Apweiler

Streyczek

Saliba

et al. 2022

IJMS

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Anti-neuroinflammatory treatment has gained importance in the search for pharmacological treatments of different neurological and psychiatric diseases, such as depression, schizophrenia, Parkinson’s disease, and Alzheimer’s disease. Clinical studies demonstrate a reduction of the mentioned diseases’ symptoms after the administration of anti-inflammatory drugs. Novel coumarin derivates have been shown to elicit anti-neuroinflammatory effects via G-protein coupled receptor GPR55, with possibly reduced side-effects compared to the known anti-inflammatory drugs. In this study, we, therefore, evaluated the anti-inflammatory capacities of the two novel coumarin-based compounds, KIT C and KIT H, in human neuroblastoma cells and primary murine microglia. Both compounds reduced PGE2-concentrations likely via the inhibition of COX-2 synthesis in SK-N-SH cells but only KIT C decreased PGE2-levels in primary microglia. The examination of other pro- and anti-inflammatory parameters showed varying effects of both compounds. Therefore, the differences in the effects of KIT C and KIT H might be explained by functional selectivity as well as tissue- or cell-dependent expression and signal pathways coupled to GPR55. Understanding the role of chemical residues in functional selectivity and specific cell- and tissue-targeting might open new therapeutic options in pharmacological drug development and might improve the treatment of the mentioned diseases by intervening in an early step of their pathogenesis.

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Section: Discussionsupporting

confidence: 53%

Functional Selectivity of Coumarin Derivates Acting via GPR55 in Neuroinflammation

Apweiler

Streyczek

Saliba

et al. 2022

IJMS

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“…PGE 2 itself further enhances COX-2 and mPGES-1 expression via EP2 receptors; thus, a reduction of PGE 2 should be accompanied by reduced COX-2 and mPGES-1 expression and synthesis [ 55 ] as well as reduced cytokine release [ 25 ] via different signaling pathways. Furthermore, the possible involvement of 8-iso-PGF 2α as a signaling molecule of the AA/COX-2 pathway should be considered and further investigated in future studies, as we have discussed previously [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

Licochalcone A Inhibits Prostaglandin E2 by Targeting the MAPK Pathway in LPS Activated Primary Microglia

et al. 2023

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Neuroinflammation and oxidative stress are conditions leading to neurological and neuropsychiatric disorders. Natural compounds exerting anti-inflammatory and anti-oxidative effects, such as Licochalcone A, a bioactive flavonoid present in a traditional Chinese herb (licorice), might be beneficial for the treatment of those disorders. Therefore, this study aimed to investigate the anti-inflammatory and anti-oxidative effects of Licochalcone A in LPS-activated primary rat microglia. Licochalcone A dose-dependently prevented LPS-induced PGE2 release by inhibiting the arachidonic acid (AA)/cylcooxygenase (COX) pathway decreasing phospholipase A2, COX-1, and COX-2 protein levels. Furthermore, LPS-induced levels of the cytokines IL-6 and TNFα were reduced by Licochalcone A, which also inhibited the phosphorylation and, thus, activation of the mitogen-activated protein kinases (MAPK) p38 MAPK and Erk 1/2. With the reduction of 8-iso-PGF2α, a sensitive marker for oxidative stress, anti-oxidative effects of Licochalcone A were demonstrated. Our data demonstrate that Licochalcone A can affect microglial activation by interfering in important inflammatory pathways. These in vitro findings further demonstrate the potential value of Licochalcone A as a therapeutic option for the prevention of microglial dysfunction related to neuroinflammatory diseases. Future research should continue to investigate the effects of Licochalcone A in different disease models with a focus on its anti-oxidative and anti-neuroinflammatory properties.

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“…Generally, this assay determines the number of metabolically active and viable cells in cell culture based on the reduction of a yellow tetrazolium salt (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide or MTT) to purple formazan in the cells. The procedure corresponded to experiments already performed and described [ 41 , 42 ].…”

Section: Methodsmentioning

confidence: 99%

Turmeric Extract (Curcuma longa) Mediates Anti-Oxidative Effects by Reduction of Nitric Oxide, iNOS Protein-, and mRNA-Synthesis in BV2 Microglial Cells

et al. 2022

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Plant-derived products have been used since the beginnings of human history to treat various pathological conditions. Practical experience as well as a growing body of research suggests the benefits of the use of turmeric (Curcuma longa) and some of its active components in the reduction of oxidative stress, a mechanism leading to neurodegeneration. In this current study, we investigated the effects of a preparation of Curcuma longa, and its constituents curcumin, tetrahydrocurcumin, and curcumenol, in one of the molecular pathways leading to oxidative stress, which is the release of NO, a free radical involved in stress conditions, using the BV2 microglial cell line. The concentration-dependent reduction of NO is linked to reduced amounts of iNOS protein- and mRNA-synthesis and is possibly mediated by the phosphorylation of mitogen-activated protein kinases (MAPK) such as p42/44 or p38 MAPK. Therefore, the use of turmeric extract is a promising therapeutic option for diseases linked to the dysregulation of oxidative stress, with fewer side-effects in comparison to the currently used pharmacotherapeutics.

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Anti-Inflammatory and Anti-Oxidative Effects of AM404 in IL-1β-Stimulated SK-N-SH Neuroblastoma Cells

Cited by 7 publications

References 53 publications

Functional Selectivity of Coumarin Derivates Acting via GPR55 in Neuroinflammation

Functional Selectivity of Coumarin Derivates Acting via GPR55 in Neuroinflammation

Licochalcone A Inhibits Prostaglandin E2 by Targeting the MAPK Pathway in LPS Activated Primary Microglia

Turmeric Extract (Curcuma longa) Mediates Anti-Oxidative Effects by Reduction of Nitric Oxide, iNOS Protein-, and mRNA-Synthesis in BV2 Microglial Cells

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