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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey
EFFECT OF RESVERATROL ON SELECTED SERUM COMPONENTS IN A RAT ENDOTOXEMIC MODEL
Abstract number: PC309
Col1 Ramazan, Keskin1 Ercan
1Department of Physiology, Faculty of Veterinary Medicine, Selcuk University, Konya/TURKEY
Objective:
Resveratrol (RES) exhibits a wide range of biological activities including anti-inflammatory and antioxidant effects. Lipopolysaccharide (LPS, endotoxin) and proinflammatory cytokines are involved in the pathogenesis of sepsis and plays a pivotal role in the initiation of tissue damage, multiple organ failure (MOF) and haemostatic disturbances. In this experimental study, our aim was to investigate the role of RES on inflammatory and biochemical disturbances in LPS-treated rats.
Methods:
A total of 60 adult male Wistar rats were divided into six equal groups: Group 1 served as negative control (C) and was infused 10 ml saline for 6 h via the tail vein of rats. Animals in Group 2 were continuously infused LPS (Escherichia Coli, 0.111:B4, 1.6 mg/100g) in 10 ml of physiological saline for 6 h. In Group 3, RES (30 mg/kg) was injected intraperitoneally and was infused 10 ml saline for 6 h. In Group 4 and 5, after RES (15 and 30 mg/kg respectively) was administrated intraperitoneally, endotoxin was infused. In group 6, before the infusion of endotoxin, RES (20 mg/kg/day) was injected intraperitoneally for 7 successive days.
Results:
LPS caused statistically significant increases in plasma TNF-a, IL-6 and IL1b levels, CRP, AST, ALT, creatinine, BUN, cholesterol, triglyceride concentration, and caused statistically significant decreases in total protein and albumin levels. RES could inhibit only serum cytokine levels (P<0.05) in group 5, However, it moderately suppressed both the levels of serum cytokines and biochemical parameters (P<0.05) in group 6.
Conclusions:
In conclusion, administration of RES may lead to potential new therapies in endotoxemia.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC309