1-Methylnicotinamide (MNA), previously considered to be a biologically inactive metabolite of nicotinamide (NA), has been recently presented as a potential anti-inflammatory agent. It has been suggested that MNA may regulate the human endothelium cell inflammatory response processes caused by external agents, such as tumor necrosis factor alpha (TNF-α). For example, the incubation of endothelial cells with TNF-α (10 ng/ml) for 1 h causes a significant increase in cell stiffness and a reduction in nitric oxide NO production. In the presented work, the anti-inflammatory potential of MNA (100 nM) was investigated using an in vitro model of endothelial cell dysfunction induced by incubation with TNF-α (10 ng/ml). Nanoindentation spectroscopy with an AFM tip, F-actin fluorescent staining and the measurement of NO production and PGI2 release were used to characterize the changes in the endothelial cell phenotype influenced by TNF-α and MNA. Therapeutic and protective effects of MNA against inflammation of the endothelium in vitro were observed by the return of measured parameters (elasticity, NO production) to the reference level. The measurements confirmed that MNA acts as an anti-inflammatory agent for endothelial cells, and this result was consistent across all 4 complementary methods used. The results using our in vitro model demonstrate that MNA can serve both as a preventive and therapeutic compound. Acknowledgements MNA has been kindly provided by Prof. Jerzy Gebicki, Technical University of Lodz. Numerous discussions with Prof. Stefan Chlopicki are gratefully acknowledged. This work was supported by the European Union from the resources of the European Regional Development Fund under the Innovative Economy Program (grant coordinated by JCET-UJ, No POIG.01.01.02-00-069/09)

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