Applications
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In mouse endothelial cells, PJ34 significantly inhibited high glucose-induced PARP activation at the doses of 0.5 and 3 μM, as well as the development of endothelial dysfunction at the dose of 3 μM. Meanwhile, PARP inhibition caused by PJ34 (3 μM) did not alter the degree of NF-κB activation. In human umbilical vein endothelial cells, PJ34 at 1 μM exhibited marked inhibitory effect on high glucose-induced PARP activation.
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Applications
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In MBP-immunized PLSJL mice, PJ34 inhibited the development of clinical signs of experimental allergic encephalomyelitis (EAE). PJ34 also suppressed the onset of EAE by reducing CNS inflammation and maintaining neurovascular integrity. In addition, PJ34 down-regulated the expression levels of TNF-α and ICAM-1 in the spinal cord tissues.
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References:
[1]. Garcia Soriano F, Virág L, Jagtap P, Szabó E, Mabley JG, Liaudet L, Marton A, Hoyt DG, Murthy KG, Salzman AL, Southan GJ, Szabó C. Diabetic endothelial dysfunction: the role of poly(ADP-ribose) polymerase activation. Nat Med. 2001 Jan;7(1):108-13.
[2]. Scott GS, Kean RB, Mikheeva T, Fabis MJ, Mabley JG, Szabó C, Hooper DC. The therapeutic effects of PJ34 [N-(6-oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide.HCl], a selective inhibitor of poly(ADP-ribose) polymerase, in experimental allergic encephalomyelitis are associated with immunomodulation. J Pharmacol Exp Ther. 2004 Sep;310(3):1053-61.
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