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Cells 2018, 7(11), 217; https://doi.org/10.3390/cells7110217

Mechanisms of TQ-6, a Novel Ruthenium-Derivative Compound, against Lipopolysaccharide-Induced In Vitro Macrophage Activation and Liver Injury in Experimental Mice: The Crucial Role of p38 MAPK and NF-κB Signaling

1
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2
Department of Chemistry, North Eastern Hill University, Shillong 793022, India
3
Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
4
School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan
*
Author to whom correspondence should be addressed.
Received: 1 October 2018 / Revised: 12 November 2018 / Accepted: 14 November 2018 / Published: 19 November 2018
(This article belongs to the Special Issue Protein Kinases: Signalling and Disease)
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Abstract

Several studies have reported that metal complexes exhibit anti-inflammatory activities; however, the molecular mechanism is not well understood. In this study, we used a potent ruthenium (II)-derived compound, [Ru(η6-cymene)2-(1H-benzoimidazol-2-yl)-quinoline Cl]BF4 (TQ-6), to investigate the molecular mechanisms underlying the anti-inflammatory effects against lipopolysaccharide (LPS)-induced macrophage activation and liver injury in mice. Treating LPS-stimulated RAW 264.7 cells with TQ-6 suppressed nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner. The LPS-induced expression of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) were reduced in TQ-6-treated cells. TQ-6 suppressed, LPS-stimulated p38 MAPK phosphorylation, IκBα degradation, and p65 nuclear translocation in cells. Consistent with the in vitro studies, TQ-6 also suppressed the expression of iNOS, TNF-α, and p65 in the mouse model with acute liver injury induced by LPS. The present study showed that TQ-6 could protect against LPS-induced in vitro inflammation in macrophage and in vivo liver injury in mice, and suggested that NF-κB could be a promising target for protecting against LPS-induced inflammation and liver injury by TQ-6. Therefore, TQ-6 can be a potential therapeutic agent for treating inflammatory diseases. View Full-Text
Keywords: RAW 264.7 cells; ruthenium compound; LPS; NF-κB; nuclear translocation; mice liver injury RAW 264.7 cells; ruthenium compound; LPS; NF-κB; nuclear translocation; mice liver injury
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Hsia, C.-H.; Velusamy, M.; Jayakumar, T.; Chen, Y.-J.; Hsia, C.-W.; Tsai, J.-H.; Teng, R.-D.; Sheu, J.-R. Mechanisms of TQ-6, a Novel Ruthenium-Derivative Compound, against Lipopolysaccharide-Induced In Vitro Macrophage Activation and Liver Injury in Experimental Mice: The Crucial Role of p38 MAPK and NF-κB Signaling. Cells 2018, 7, 217.

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