PARP Activation And Plasma Inflammatory Cytokines In ACS

Background: Poly(ADP-ribose) polymerase-1 (PARP-1) takes part in the transcriptional regulations of some cytokines. To study the alteration of PARP activity in circulated mononuclear cell (MNC) will help us to explain the increase of plasma cytokines in acute coronary syndrome (ACS).Objectives: To explore the relationship between poly(ADP-ribose) polymerase-1 (PARP-1) activation of circulated mononuclear cell (MNC) and the increases in plasma tumor necrosis factor-α(TNF-α) ,interleukin-10 (IL-10) and interleukin-6 (IL-6) in ACS.Methods: 46 patients in different time points after AMI, 46 patients with unstable angina pectoris, 10 patients with stable angina pectoris and 20 healthy people were enrolled in this study. PARP-1 activity was measured with universal colorimetric PARP assay kit. Plasma TNF-α, IL-10 and IL-6 were measured with ELISA. Left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) were measured with echocardiography.Results: PARP-1 activity of circulating MNC increased significantly in all ACS patients. The peak mean PARP-1 activity was presented in patients at 3 days after AMI and was about 4.08 times the stable angina pectoris control level or 4.67 times the healthy control level. PARP-1 activity of circulating MNC had no significant differences in SAP patients and healthy controls. Plasma TNF-α, IL-10 and IL-6 increased significantly in all ACS patients, however, plasma IL-6 in post AMI patients at the 4 weeks decreased as low as healthy controls. PARP-1 activity of MNC correlated positively with plasma TNF-αlevel, IL-10 level, IL-6 level and with the ratio of TNF-α/IL-10 respectively. MNC PARP-1 activity correlated negatively with left ventricular ejection fraction (LVEF) and fractional shortening (LVSF) of patients who got echocardiography measurement and blood sample collection in the same day.Conclusion: In ACS, increases in plasma TNF-α, IL-10 and IL-6 are associated with the activation of PARP-1 of circulating MNC. PARP-1 may be one of the regulatory mechanisms in such inflammatory response.