Bahador Bagheri1, Bahram Sohrabi2, Ali Akbar Movassaghpour3, Simin Mashayekhi4, Afagh Garjani5, Mehriar Shokri2, Masoud Pezeshkian2, Alireza Garjani1. 1. Dept. of Pharmacology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran. 2. Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz, Iran. 3. Hematology Research Centre, Tabriz University of Medical Sciences, Tabriz, Iran. 4. Dept. of Clinical Pharmacy, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran. 5. School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
BACKGROUND: 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-α and IL-1β 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-α and IL-1β 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.
BACKGROUND: 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 humanTLR4 (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-α and IL-1β 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-α and IL-1β 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.
Authors: B L van der Hoeven; N M M Pires; H M Warda; H Putter; P H A Quax; M J Schalij; J W Jukema Journal: Int J Cardiol Date: 2007-04-03 Impact factor: 4.164
Authors: D Versteeg; I E Hoefer; A H Schoneveld; D P V de Kleijn; E Busser; C Strijder; M Emons; P R Stella; P A Doevendans; G Pasterkamp Journal: Heart Date: 2007-08-08 Impact factor: 5.994