The anti-inflammatory effects of platinum nanoparticles on the lipopolysaccharide-induced inflammatory response in RAW 264.7 macrophages

Rehman, Mati Ur; Yoshihisa, Yoko; Miyamoto, Yusei; Shimizu, Tadamichi

doi:10.1007/s00011-012-0512-0

Cited by 92 publications

(80 citation statements)

References 67 publications

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“…The anti-oxidant properties of CeO 2 NPs thus depend on the nanocrystal diameter (Lee et al, 2013) and the ratio of surface Ce 3+ /Ce 4+ (Das et al, 2012). This interesting anti-oxidant property of some nanomaterials is intended to be used in nanomedical applications (Colon et al, 2010, Rehman et al, 2012). …”

Section: 2 Hierarchical Oxidative Stress Modelmentioning

confidence: 99%

Intracellular Signal Modulation by Nanomaterials

Hussain

Garantziotis

Rodrigues‐Lima

et al. 2014

Advances in Experimental Medicine and Biology

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A thorough understanding of the interactions of nanomaterials with biological systems and the resulting activation of signal transduction pathways is essential for the development of safe and consumer friendly nanotechnology. Here we present an overview of signaling pathways induced by nanomaterial exposures and describe the possible correlation of their physicochemical characteristics with biological outcomes. In addition to the hierarchical oxidative stress model and a review of the intrinsic and cell-mediated mechanisms of reactive Oxygen species (ROS) generating capacities of nanomaterials, we also discuss other oxidative stress dependent and independent cellular signaling pathways. Induction of the inflammasome, calcium signaling, and endoplasmic reticulum stress are reviewed. Furthermore, the uptake mechanisms can crucially affect the cytotoxicity of nanomaterials and membrane-dependent signaling pathways can be responsible for cellular effects of nanomaterials. Epigenetic regulation by nanomaterials effects of nanoparticle-protein interactions on cell signaling pathways, and the induction of various cell death modalities by nanomaterials are described. We describe the common trigger mechanisms shared by various nanomaterials to induce cell death pathways and describe the interplay of different modalities in orchestrating the final outcome after nanomaterial exposures. A better understanding of signal modulations induced by nanomaterials is not only essential for the synthesis and design of safer nanomaterials but will also help to discover potential nanomedical applications of these materials. Several biomedical applications based on the different signaling pathways induced by nanomaterials are already proposed and will certainly gain a great deal of attraction in the near future.

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Section: 2 Hierarchical Oxidative Stress Modelmentioning

confidence: 99%

Intracellular Signal Modulation by Nanomaterials

Hussain

Garantziotis

Rodrigues‐Lima

et al. 2014

Advances in Experimental Medicine and Biology

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“…In pathogenic conditions, abnormally activated macrophages produce excessive amounts of various proinflammatory mediators and cytokines that eventually aggravate inflammatory conditions. Lipopolysaccharides (LPSs), a component of the outer membrane of Gram-negative bacteria, are the most common cause of macrophage activation [2][3]. LPS-induced activation of macrophages causes a wide range of pro-inflammatory responses, such as production of pro-inflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Morus Root Extract (MRE) Against Lipopolysaccharide-Activated RAW264.7 Cells and CCl4-Induced Mouse Hepatic Damage

Tseng

Lin

Chang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Inflammation is one of the main contributors to chronic diseases such as cancer. It is of great value to identify the potential activity of various medicinal plants for regulating or blocking uncontrolled chronic inflammation. We investigated whether the root extract of Morus australis possesses antiinflammatory and antioxidative stress potential and hepatic protective activity. Methods: The microwave-assisted extractionwere was used to prepare the ethanol extract from the dried root of Morus australis (MRE), including polyphenolic and flavonoid contents. Lipopolysaccharide (LPS)-stimulated RAW264.7 cells was examined the anti-inflammatory and anti-oxidative potential of MRE. CCl₄-induced mouse hepatic damage were performed to detect the hepatic protective potential in vivo. Immunohistochemistry (IHC) and western blot assays were used to detect target proteins. Results: MRE contained approximately 23% phenolic compounds and 3% flavonoids. The major flavonoid component of MRE was morusin. MRE and morusin inhibited lipopolysaccharide-induced production of nitrite and prostaglandin E2 in RAW264.7 cells. MRE and morusin also suppressed the formation of intracellular reactive oxygen species and the expression of iNOS and COX-2. In an in vivo study, a thiobarbituric acid reactive substances assay showed that MRE inhibited CCl₄-induced oxidative stress and expression of nitrotyrosine. MRE also decreased CCl₄-induced hepatic iNOS and COX-2 expression, as well as CCl₄-induced hepatic inflammation and necrosis in mice. Conclusion: MRE exhibited antiinflammatory and hepatic protective activity.

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“…Macrophages play essential roles in the host defense against bacterial infection (Rehman et al , 2012). However, aberrant activation of macrophages plays detrimental roles in multiple inflammation-related disorders including sepsis by producing a wide range of pro-inflammatory mediators and cytokines (Rietschel and Brade, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Although macrophages play essential roles in the mobilization of the host defense against bacterial infection (Rehman et al , 2012), aberrant activation of macrophages has been also reported to play pathogenic roles in various inflammatory disorders including sepsis (Kim et al , 2012). In pathogenic conditions, abnormally activated macrophages produce excessive amount of a variety of pro-inflammatory mediators and cytokines that eventually aggravates the inflammatory conditions (Itharat and Hiransai, 2012).…”

Section: Introductionmentioning

confidence: 99%

N-(p-Coumaryol)-Tryptamine Suppresses the Activation of JNK/c-Jun Signaling Pathway in LPS-Challenged RAW264.7 Cells

Lee

Park

et al. 2014

Biomolecules & Therapeutics

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N-(p-Coumaryol) tryptamine (CT), a phenolic amide, has been reported to exhibit anti-oxidant and anti-inflammatory activities. However, the underlying mechanism by which CT exerts its pharmacological properties has not been clearly demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of CT in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells. CT significantly inhibited LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and PGE2, and protein expressions of iNOS and COX-2. In addition, CT significantly suppressed LPS-induced secretion of pro-inflammatory cytokines such as TNF-α and IL-1β. To elucidate the underlying anti-inflammatory mechanism of CT, involvement of MAPK and Akt signaling pathways was examined. CT significantly attenuated LPS-induced activation of JNK/c-Jun, but not ERK and p38, in a concentration-dependent manner. Interestingly, CT appeared to suppress LPS-induced Akt phosphorylation. However, JNK inhibition, but not Akt inhibition, resulted in the suppression of LPS-induced responses, suggesting that JNK/c-Jun signaling pathway significantly contributes to LPS-induced inflammatory responses and that LPS-induced Akt phosphorylation might be a compensatory response to a stress condition. Taken together, the present study clearly demonstrates CT exerts anti-inflammatory activity through the suppression of JNK/c-Jun signaling pathway in LPS-challenged RAW264.7 macrophage cells.

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The anti-inflammatory effects of platinum nanoparticles on the lipopolysaccharide-induced inflammatory response in RAW 264.7 macrophages

Abstract: These results suggest that the anti-inflammatory properties of nano-Pt may be attributed to their downregulation of the NFκB signaling pathway in macrophages, thus supporting the use of nano-Pt as an anti-inflammatory agent.

Cited by 92 publications

References 67 publications

Intracellular Signal Modulation by Nanomaterials

Intracellular Signal Modulation by Nanomaterials

Protective Effects of Morus Root Extract (MRE) Against Lipopolysaccharide-Activated RAW264.7 Cells and CCl4-Induced Mouse Hepatic Damage

N-(p-Coumaryol)-Tryptamine Suppresses the Activation of JNK/c-Jun Signaling Pathway in LPS-Challenged RAW264.7 Cells

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