Effects of Resolvin D1 on Tumor Necrosis Factor-Induced Phosphorylation of the Mitogen Activated Protein Kinase in the Rat C6 Glioma Cells,SALLY A.M. ABD EL-MOATY, YASSER M. MOUSTAFA, EL-SAYED E. EL-AWADY, ALAA EL-DIN S. ABD EL-HAMID and ERNST BRODIN
Abstract
Introduction and Aim of theWork: Resolution of inflam-mation is an active process involving the action of anti-inflammatory lipid mediators. Recently a family of pro-resolving anti-inflammatory lipid mediators known as resolvins was identified. Resolvins are derived from the omega-3 polyunsaturated fatty acids and have shown beneficial effects in various disease models with inflammatory components. Resolvins were shown to reduce pain in different animal models. In order to understand the molecular mechanisms of action of resolvins the current study aimed at investigating if resolvin D1 can interfere with the activation of mitogen activated protein kinase pathway in the rat C6 glioma cell; moreover, the expression of the resolvin E1 receptor, cmklr1 was assessed in the same cells.
Material and Methods: Rat C6 glioma cell cultures were pretreated with resolvin D1, and changes in the levels of phosphorylated mitogen activated protein kinases, P38, ERK, and JNK in response to tumor necrosis factor stimulation were assessed using Western blotting. Furthermore, changes in the levels of CMKLR1 in response to tumor necrosis factor stimulation were followed using Western blotting in the same type of cells.
Results and Conclusion: Resolvin D1 pretreatment atten-uated the tumor necrosis factor-induced activation of the JNK but not the P38 or ERK mitogen activated protein kinases in the rat C6 glioma cells. This suggests a new mechanism through which resolvin D1 is acting. Additionally, CMKLR1, the resolvin E1 receptor was constitutively expressed in the rat C6 glioma cells and the levels were increased following 3 hours stimulation with tumor necrosis factor.