Synthesis of a Novel Cyclic Prodrug of <i>S</i>-Allyl-glutathione Able To Attenuate LPS-Induced ROS Production through the Inhibition of MAPK Pathways in U937 Cells

Patruno, Antonia; Fornasari, Erika; Stefano, Antonio Di; Cerasa, Laura Serafina; Marinelli, Lisa; Baldassarre, Leonardo; Sozio, Piera; Türkez, Hasan; Franceschelli, Sara; Ferrone, Alessio; Giacomo, Viviana di; Speranza, Lorenza; Felaco, Mario; Cacciatore, Ivana

doi:10.1021/mp500431r

Cited by 32 publications

(15 citation statements)

References 48 publications

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“…It is well-known that inflammation induced by endotoxin such as LPS was closely associated with ROS generation ( Patruno et al, 2015 ). ROS, which are mainly produced by NADPH oxidase, are commonly considered cytotoxic and can even induce cell damage in high levels ( Ray et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

et al. 2018

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Acute lung injury (ALI) is a progressive clinical disease with a high mortality rate, and characterized by an excessive uncontrolled inflammatory response. MicroRNAs (miRNAs) play a critical role in various human inflammatory diseases, and have been recognized as important regulators of inflammation. However, the regulatory mechanisms mediated by miRNAs involved in Lipopolysaccharide (LPS)-induced inflammation in ALI remain hazy. In this study, we found that miR-181a expression in the lung tissues of ALI mice and LPS-stimulated RAW 264.7 macrophages is dramatically reduced. We also show that over-expression of miR-181a significantly decreased the production of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, whereas inhibition of miR-181a reversed this decrease. Moreover, miR-181a inhibits NF-κB activation and accumulation of reactive oxygen species (ROS) by targeting TLR4 expression. We further verify that miR-181a suppresses TLR4 expression by binding directly to the 3′-UTR of TLR4. Therefore, we provide the first evidence for the negative regulation of miR-181a in LPS-induced inflammation via the suppression of ROS generation and TLR4-NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

et al. 2018

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“…As described previously [43], to each well were added: 100 µL PBS (pH 7.8, 50 mM), 5 µL catalase, 25 µL NBT (5.6 × 10 −9 M), 50 µL xanthine (0.1 mM), 50 µL xanthine oxidase (0.1 mM) and LicoC (1–250 µM). Following the addition of NBT, the plates were incubated at RT for 1 h, and the amount of NBT formazan was quantified at 560 nm.…”

Section: Methodsmentioning

confidence: 99%

Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation

Franceschelli

Pesce

Ferrone

et al. 2017

IJMS

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Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation.

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“…This assay is used to detect the superoxide dismutation potential of the ERW. As described previously, cells were seeded on to 96-well culture plates at concentrations of 5 × 10 5 mL −1 [ 39 ]. The following were added to each well: 100 μL potassium phosphate buffer, pH 7.8 (50 mM), 5 μL catalase, 25 μL NBT (5.6 × 10 −9 M), 50 μL xanthine (0.1 mM), 50 μL xanthine oxidase (0.1 mM).…”

Section: Methodsmentioning

confidence: 99%

New Approach in Translational Medicine: Effects of Electrolyzed Reduced Water (ERW) on NF-κB/iNOS Pathway in U937 Cell Line under Altered Redox State

Franceschelli

Gatta

Pesce

et al. 2016

IJMS

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It is known that increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) can exert harmful effects, altering the cellular redox state. Electrolyzed Reduced Water (ERW) produced near the cathode during water electrolysis exhibits high pH, high concentration of dissolved hydrogen and an extremely negative redox potential. Several findings indicate that ERW had the ability of a scavenger free radical, which results from hydrogen molecules with a high reducing ability and may participate in the redox regulation of cellular function. We investigated the effect of ERW on H2O2-induced U937 damage by evaluating the modulation of redox cellular state. Western blotting and spectrophotometrical analysis showed that ERW inhibited oxidative stress by restoring the antioxidant capacity of superoxide dismutase, catalase and glutathione peroxidase. Consequently, ERW restores the ability of the glutathione reductase to supply the cell of an important endogenous antioxidant, such as GSH, reversing the inhibitory effect of H2O2 on redox balance of U937 cells. Therefore, this means a reduction of cytotoxicity induced by peroxynitrite via a downregulation of the NF-κB/iNOS pathway and could be used as an antioxidant for preventive and therapeutic application. In conclusion, ERW can protect the cellular redox balance, reducing the risk of several diseases with altered cellular homeostasis such as inflammation.

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Synthesis of a Novel Cyclic Prodrug of S-Allyl-glutathione Able To Attenuate LPS-Induced ROS Production through the Inhibition of MAPK Pathways in U937 Cells

Cited by 32 publications

References 48 publications

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation

New Approach in Translational Medicine: Effects of Electrolyzed Reduced Water (ERW) on NF-κB/iNOS Pathway in U937 Cell Line under Altered Redox State

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