Ramazan Col

Effect of recombinant interleukin-10 on some haematological and biochemical parameters in a rat endotoxaemic model.

Recombinant interleukin-10 (rIL10) has been found to suppress the synthesis of tumour necrosis factor (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6) and tissue factor and to improve survival from experimental sepsis. The aim of this study was to evaluate the protective effect of rIL-10 on lipopolysaccharide-(LPS-) induced haematological and biochemical disturbances in rats. In the present study, 40 rats were used and divided equally into four 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 rIL10 treatment (125 μg/kg) 2 min before 0.9% saline injection, Group 4 received rIL10 treatment 2 min before endotoxin treatment. When compared with the controls, platelet count, leukocyte count (with a marked neutrophilia and lymphopenia) and fibrinogen were decreased, while activated partial thromboplastin time (APTT) and prothrombin time (PT) were prolonged in the endotoxaemic rats. In addition, LPS caused statistically significant increases in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities as well as creatinine, cholesterol and triglyceride concentrations, while it caused a statistically significant decrease in glucose, total protein and albumin levels as compared to the control group. On the other hand, rIL10 significantly suppressed disturbances in the haematological and biochemical parameters associated with endotoxaemia. As a result, rIL10 may be efficacious in preventing haematological disorders, tissue damage and changes in lipid, protein and carbohydrate metabolism in endotoxaemia.

Effect of Vasoactive Intestinal Peptide (VIP) on Cytokine Levels and Haemostatic and Biochemical Parameters in A Rat Endotoxaemic Model

Abstract The presented study was planned to determine whether vasoactive intestinal peptide (VIP) could prevent cytokine haemostatic, haematological, and biochemical disturbances in LPS-treated rats. Adult male Wistar rats (weight range: 200-250 g) were used. The study included four groups: group 1 served as a control group (C); animals in group 2 were given intravenously 1.6 mg/100 g of LPS (E. coli, serotype 0.111:B4); in group 3, rats were injected intraperitoneally with 25 ng/kg of VIP; in group 4, the same doses of VIP and LPS were injected simultaneously. Blood samples were collected 6 h after treatments. In endotoxaemic rats, platelet count, fibrinogen, and antithrombin levels were decreased, the activated partial thromboplastin time and prothrombin time were prolonged, and leucopoenia, as well as significant changes in differential leukocyte percentage were demonstrated. In addition, LPS caused statistically significant increases in plasma TNF- , IL-6, and IL-10 levels, and AST, ALT, creatinine, cholesterol, triglyceride concentrations. However, it caused a statistically significant decrease in total protein and albumin levels when compared to control group. The results showed that during endotoxaemia, VIP had moderately therapeutic effect as an antiinflammatory agent, suppressing TNF-α and IL-6, and stimulating IL-10; however, it was not effective against the adverse effect of LPS on investigated haematological and biochemical parameters.