Novel TSPO Ligand 2-Cl-MGV-1 Can Counteract Lipopolysaccharide Induced Inflammatory Response in Murine RAW264.7 Macrophage Cell Line and Lung Models
Fadi Obeid,
Meygal Kahana,
Baraah Dahle,
Sheelu Monga,
Yaniv Zohar,
Abraham Weizman,
Moshe Gavish
Affiliations
Fadi Obeid
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
Meygal Kahana
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
Baraah Dahle
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
Sheelu Monga
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
Yaniv Zohar
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
Abraham Weizman
Laboratory of Biological and Molecular Psychiatry, Felsenstein Medical Research Center, Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
Moshe Gavish
Ruth and Bruce Rappaport Faculty of Medicine, Technion—Israel Institute of Technology, Haifa 31096, Israel
We assessed the anti-inflammatory activity of the TSPO ligand 2-Cl-MGV-1. Lipopolysaccharide (LPS) was used to induce inflammatory response in a murine RAW264.7 macrophage model (LPS: 100 ng/mL) and a mouse model (C57BL/6) of lung inflammation (LPS: 5 mg/kg). In the macrophage model, the presence of 2-Cl-MGV-1 (25 µM) caused the LPS-induced elevation in nitrite levels to decrease by 70% (p p p p p p p p < 0.05) when administered 1 h after LPS. All cytokine assessments were conducted 6 h post LPS injection. Histological analyses showed decreased leukocyte adherence in the lung tissue of the ligand-treated mice. 2-Cl-MGV-1 administration 30 min prior to exposure to LPS inhibited inflammation-induced open field immobility. The beneficial effect of 2-Cl-MGV-1 suggests its potential as a therapeutic option for inflammatory diseases.
