Effects of Platelet-activating Factor Receptor Antagonist (PAFRA) on Selected Inflammatory and Biochemical Parameters in Lipopolysaccharide-Induced Rat Endotoxemia Model

Platelet-activating factor (PAF) is a significant phospholipid mediator of the immune system produced by a veriety of cells involved in inflammatory reactions in sepsis. In this experimental study, our aim was to investigate the role of PAF receptor antagonist (PAFRA) on biochemical and inflammatory disturbances in lipopolysaccharide (LPS)-treated rats. A total of 32 adult male Wistar rats were divided into four equal groups: Group 1 (control group, C) was treated with 0.9% saline. Group 2: LPS was injected intravenously (1.6 mg/100 g), Group 3 received PAFRA treatment (10 mg/kg) 2 min before 0.9% saline injection, Group 4 received PAFRA treatment 2 min before endotoxin treatment. Blood samples were collected 6 h after treatment. LPS (Group-II) caused statistically significant increases in serum TNF-a, IL-6 and IL1β levels, CRP, LDH, AST, ALT, creatinine, BUN, cholesterol, triglyceride concentration, and caused statistically significant decreases in platelet count, glucose, total protein and albumin levels. Also, when compared to control group leukopenia and significant changes in the leukocyte differential were evident. In group 4, PAFRA inhibited serum TNF-α and IL1β levels, leukopenia compared with the group 2 (P<0.05). However, there were no significant differences in the other parameters between the two groups. The results demonstrate that at the administered dose and route, PAFRA has a slight effect in the pathogenesis of endotoxemia.