Background Ellagic acid (EA) is a phenolic constituent in fruits and nuts, such as raspberries, strawberries, walnuts, mango kernel and pomegranate. It was documented that EA shows anti-fibrotic, anti-inflammatory activity in vivo model of bowel inflammation and lung fibrosis, however the precise mechanism of signal inhibition was not extensively investigated. Objectives The objectives of this study are first, to elucidate the anti-inflammatory effect of EA in RAW 264.7 murine macrophage cell line by NF-kB pathway in vitro, and second, to compare it with effect of other immuno-modulating agent, tacrolimus and colchicine. Methods We determined the cytotoxic effect of EA using MTT assay. The effects of EA on tumor necrosis facor (TNF)-alpha induced mRNA and protein expression were investigated using quantitative real-time PCR and western blot. In addition, we examined the effects of pharmaceutical drugs with anti-inflammatory properties on expression of TNF-alpha. Results EA significantly suppressed the expression of interleukin-1 beta and TNF-alpha in a dose dependent manner. EA suppressed TNF-alpha induced inflammatory genes expression by inhibiting the phosphorylation of JNK and Akt, whereas had no significant effect on p38 activation. In addition, the inhibitory effect of EA on TNF-alpha induced inflammatory genes expression was regulated by suppression of IkB-alpha phosphorylation and NF-kB translocation. The expression of TNF-alpha mRNA level was reduced comparably treated with EA and other anti-inflammatory agents (ascorbic acid, dexamethasone and colchicine). Conclusions These findings suggest that EA suppresses inflammatory genes expression through phosphorylation of JNK/Akt and regulation of NF-kB signal pathway in TNF-alpha induced inflammation. Further investigation regarding effects of EA on autoimmune, inflammatory is scheduled. References S. Corbett, J. Daniel, R. Drayton, M. Field, R. Steinhardt, N. Garrett, Evaluation of the anti-inflammatory effects of ellagic acid, J. Perianesth. Nurs. 25 (2010), 214–220. S. Ahmed, A. Rahman, M. Saleem, M. Athar, S. Sultana, Ellagic acid ameliorates nickel induced biochemical alterations: diminution of oxidative stress, Hum. Exp. Toxicol. 18 (1999) 691–698. Disclosure of Interest None declared

Background Pulmonary arterial hypertension (PAH) is a major cause of mortality in connective tissue disease (CTD). Objectives The survival rates and mortality-predictive factors of a nationwide registry of Korean patients with CTD-PAH were determined. Methods Patients with CTD-PAH were enrolled between April 2008 and December 2012. Hemodynamic parameters and clinical data (WHO-functional class [FC], organ involvement, laboratory tests, and treatment agents) were recorded. Survival rates were calculated by using the Kaplan–Meier method. Mortality-associated factors were examined by Cox proportional hazards regression analysis. Results In total, 174 incident PAH cases (61 with systemic lupus erythematosus, 50 with systemic sclerosis, 10 with mixed CTD, 22 with rheumatoid arthritis [RA], and 31 with other CTDs) were diagnosed by right heart catheterisation or Doppler echocardiography. Of these, 25 (14%) died during the 3.8±2.7 year follow-up period after PAH diagnosis. The 1 and 3 year survival rates were 90.7% and 87.3%, respectively. Compared to the other CTD-PAHs, RA-PAH had the lowest survival rates (56% 3 year survival; p=0.022). Multiple regression analysis revealed that low DLCO, pleural effusion, and diabetes mellitus were poor prognostic factors (p=0.008, 0.04, and 0.009, respectively). Anti-UI-RNP antibody positivity was protective (p=0.022). In patients with WHO-FC III/IV, patients who received vasodilators had lower mortality than those who did not (p=0.038). Conclusions In Korean patients with CTD-PAH, the 3 year survival rate was 87%. Low DLCO, pleural effusion, and DM were independent poor prognostic factors. Anti-UI-RNP antibody was protective. Prompt PAH-specific vasodilator therapy may improve the survival of patients with severe CTD-PAH. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.1271