Abstract
Reactive oxygen species (ROS) play major role in inducing inflammation and related diseases. Our previous studies have revealed that the ruthenium (II)-compound, [Ru(η6-cymene)2-(1H-benzoimidazol-2-yl)-quinoline Cl]BF4 (TQ-6), inhibits hydroxyl radical (OH•) formation in human platelets. TQ-6 also have protective effect against induced inflammation in macrophages and hepatic injury in mice through NF-κB signaling. However, the free radical formation inhibitory mechanism of TQ-6 in macrophages is unclear. Therefore, this study detected the antioxidative ability of TQ-6 in both a cell-free system and in LPS-induced macrophages through electron spin resonance (ESR) spectrometry. TQ-6 reduced 1,1-diphenyl-2-picrylhydrazyl (DPPH), galvinoxyl, and superoxide radicals in a cell-free system and OH• formation in macrophages. Additionally, TQ-6 activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and upregulated the antioxidant protein heme oxygenase-1 (HO-1) to elevate anti-inflammatory activity in LPS-induced macrophage cells and inhibited carrageenan-induced paw edema in a rat model. Therefore, TQ-6 may prevent oxidative stress and also act as an effective therapeutic agent for the treatment of oxidant-related diseases.
Highlights
These results indicated that TQ-6 showed stronger scavenging activity against DPPH and galvinoxyl radicals
TQ-6 is more potent on scavenging galvinox radical than DPPH. These results indicated that TQ-6 showed stronger scavenging activ against DPPH and galvinoxyl radicals
This study analyzed the antioxidative role of TQ-6 in cell-free and RAW 264.7 cell model systems by using electron spin resonance (ESR) in vitro and its anti-inflammatory properties in rat paw edema model in vivo
Summary
Oxidative stress induce inflammation via reactive oxygen species (ROS) formation, which are reflected the strong inflammatory mediators. Several ROS are produced inside lipopolysaccharide (LPS)-stimulated macrophages, such as the superoxide radical anion, which is produced primarily, but not exclusively, by NADPH oxidase (NOX) [1]. NOX is present in various cells, especially specialized phagocytic and endothelial cells [1]. Polymorphonuclear neutrophils lead to increased ROS production at the site of inflammation, resulting in endothelial dysfunction and tissue damage [2]. An antioxidant drug may be an anti-inflammatory drug and vice versa
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