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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.

TQ-6, a Novel Ruthenium Derivative Compound, Possesses Potent Free Radical Scavenging Activity in Macrophages and Rats