Rheumatoid arthritis (RA) is one of the major autoimmune diseases of global prevalence. Irrespective of much research in RA disease， no drugs with capable safety profiles are yet available. Poly(ADP-ribose) polymerase-1 (PARP-1) synthesizes and transfers ADP ribose polymers to target proteins， and regulates DNA repair and genomic integrity maintenance. PARP-1 also plays a crucial role in the progression of the inflammatory response， and its inhibition confers protection in several models of inflammatory disorders. We investigated the possible anti-arthritic effects of the PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ) in a mouse model of adjuvant induced arthritis (AIA). In this study， we examined the effects of 5-AIQ on the key mediators of arthritic inflammation， namely， edema and arthritic score， T cell subsets， regulatory T (Treg) cells， IL-17A， GITR expressing cells， NF-kB p65， IkB-α and pro and anti-inflammatory mediators mRNA expression levels. PARP-1 inhibition 5-AIQ treatment significantly attenuated the severity of AIA， reduced the arthritis scores， a substantial reduction in the levels of T cell subsets， IL-17A， NF-kB p65， GITR expressing cells， and as well as the pro-inflammatory mediators. However， 5-AIQ significantly up-regulated the number of Tregs cells， IkB-α levels and mRNA expression of anti-inflammatory mediators. Our results suggest that treatment with 5-AIQ attenuated AIA in mice might offer a promising alternative/adjunct treatment for RA.