Gram-negative bacteria have a wall surfaced with endotoxin, a lipopolysaccharide (LPS), which is released during bacterial lysis. Endotoxin is extremely active biologically, can lead to the release of free radicals, which cause tissue damage e.g. multiple organ failure The aim of the present study was to investigate the effects of evening primrose oil on LPS-induced multiple organ failure and related mechanisms
A group of male rats received lipopolysaccharide (LPS) (20 mg/kg, intraperitoneally). A second group was treated with evening primrose oil (EPO) (8 ml/kg, p.o.,daily) for four weeks followed by administration of LPS (20 mg/kg, intraperitoneally) A third group received EPO (8ml/kg. orally) for four weeks followed by intrapentoneal injection of saline. A fourth group received salıne intraperitoneally and served as control.
Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (T.bil), blood urea nitrogen (BUN) and creatinine were determined. Plasma lipid peroxidation (LPO) was analyzed using commercial kit. Nitric oxide (NO) production was estimated by Griess reaction Liver and kidney glutathione contents (GSH) were determined.
Lipopolysaccharide administration induced a significant increase in serum ALT, AST, BUN, T.bil , and creatinine levels. In addition, it induced a significant increase in plasma lipid peroxidation and nitric oxide. While, glutathione contents of liver and kidney were signıficantly reduced as a result of LPS administration. Pretreatment of rats with evening primrose oil attenuated LPS- induced hepatic and renal damage Moreover, evening primrose oil significantly decreased LPS-induced plasma lipid peroxidation and significantly increased kidney and liver GSH contents compared to LPS alone -treated rats. On the other hand, evening primrose oil had no significant effect on LPS-induced nitric oxide production Treatment of rats with EPO for four weeks had no significant effect on any of measured parameters.
In conclusion, data indicated that evening primrose oil attenuated LPS-induced multiple organ failure at least in part through its antioxidant effect