Author/Authors :
باقري ، بهادر 1347 نويسنده علوم انساني , , سهرابي، بهرام نويسنده Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz Sohrabi, Bahram , موثقپور، علي اكبر نويسنده استاديار هماتولوژي آزمايشگاهي و بانك خون ، دانشگاه علوم پزشكي تبريز، مركز تحقيقات خون و انكولوژي , , مشايخي، سيمين نويسنده , , گرجاني، آفاق نويسنده School of Medicine, Tabriz University of Medical Sciences, Tabriz Garjani, Afagh , شكري، مهريار نويسنده Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz Shokri, Mehriar , پزشكيان، مسعود نويسنده , , گرجاني ، عليرضا 1339 نويسنده پزشکي ,
Abstract :
Bacground: Evidence from several lines of investigations suggests that Toll-like receptor 4 (TLR4) is involved in atherosclerosis as a bridge between innate and acquired immunity. Percutaneous coronary intervention (PCI) can trigger inflammation through activation of human TLR4 (hTLR4) on monocytes. Hydrocortisone as an anti-inflammatory and immuno-suppressant agent has multiple mechanisms of action. In this study, we aimed at assessing the effects of hydrocortisone on monocyte expression and activity of hTLR4 in patients underwent PCI. Methods: Blood samples were taken from a total of 71 patients with chronic stable angina who were scheduled for a PCI, before the intervention. Thirty patients received 100 mg hydrocortisone prior to the procedure. Control group was composed of 41 patients underwent PCI without receiving hydrocortisone. Blood collection was repeated 2 and 4 h after PCI. The expression of hTLR4 on the surface of CD14+ monocytes and the serum levels of TNF-? and IL-1B were measured using flowcytometry and Sandwich ELISA. Results: Compared with controls, hydrocortisone significantly reduced monocyte expression of hTLR4 in test group (P < 0.01). In addition, it had a significant effect on reduction of serum concentrations of TNF-? and IL-1B in test group in a time-dependent manner (P < 0.01). Conclusion: In this study, hydrocortisone was able to reduce the hTLR4/CD14 positive monocytes and its related pro-inflammatory cytokines, thus it can decrease inflammatory responses following PCI. Iran. Biomed. J. 18 (2): 76-81, 2014