NCS 613, a PDE4 inhibitor, by increasing cAMP level suppresses systemic inflammation and immune complexes deposition in kidney of MRL/lpr lupus- prone mice

Nephritis remains the most common severe manifestation of systemic lupus erythematosus in which auto-antibodies mediate chronic inflammation and kidney damage. cAMP-phosphodiesterases regulate sodium excretion various tissues. How cAMP elevation can reduce suppress damage elusive. PDE4 signaling metabolism were investigated along immune complex depositions target tissues (histology). SLE disease progression is associated with changes activity expression. Moreover, prone mice exhibit low level to induction relocation nuclear cytoskeleton isoforms. Auto-antibodies-induced was attested by mesangial proliferation cellular infiltration. Interestingly, we reported that NCS 613 treatment decreases auto-antibody secretion their corresponding deposition Furthermore, able increase levels kidney; hence this compound rescues alterations treated mice. overcomes improving wellbeing decreasing The inhibitor, 613, a new anti-inflammatory believed be leading drug candidate for inflammatory diseases such as nephritis.