The effect of endocannabinoids on apoptosis in ''experimental sepsis model'' on mice
Abstract number: 1734_3
Kilic D., Aydos T.R., Keskil Z., Bozdogan O., Andic F., Korkut O., Edremitlioglu M.
Purpose: To investigate the apoptotic changes in renal tissues of septic mice and the effects of cannabinoid receptor antagonist (AM 630) and agonists (anadamid and WIN 55,212-2) on these changes.
Materials and Method: In this study, 56 healthy Swiss albino mice weighing 2535 g. The mice were randomly divided into 8 groups: control, sham, sepsis, sepsis treated with anandamide or WIN 55,212-2 or AM 630 and sepsis treated with ethanol or DMSO. Sepsis was induced by cecal ligation and puncture (CLP) under ketamine/xylazine anaesthesia. After 48 hours, the mice were treated intraperitoneally with anandamide (5 mg/kg) or its solvent ethanol, WIN 55,212-2 (5 mg/kg), AM 630 (1 mg/kg) or DMSO which is used as the solvent of both. Ten minutes later, the abdomen was incised and periton culture specimen was taken to confirm the existence of sepsis. The kidneys were harvested and fixed in 10% neutral formolin solution. The apoptotic changes in glomerulus, proximal and distal tubulus, and collecting ducts were determined using TUNEL method.
Findings: Neither one of sepsis, anandamide, WIN 55,212-2, AM 630, ethanol or DMSO caused any apoptotic effects on glomerulus. The induced sepsis caused an increase of apoptosis on proximal and distal tubulus. In these parts of kidney, while anandamide, WIN 55,212-2, ethanol or DMSO did not make any changes, AM 630 caused a decline in apoptosis. In the collecting ducts; groups of sepsis, anandamide, WIN 55,212-2 and AM 630 did not show any differences than the sham group.
Results: In consistency with other studies indicating the inducement of apoptosis by endotoxin in some tissues; sepsis, induced by CLP in mice renal proximal and distal tubulus, showed apoptotic effects in this study. While anadamide and WIN 55,212-2 did not cause any changes in this effect, CB2 cannabinoid receptor antagonist AM 630 caused a decline in apoptosis. In renal glomerulus, apoptotic changes did not increase.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
|Back to top|