1,721,037 research outputs found
Topical and Systemic Cannabidiol Improves Trinitrobenzene Sulfonic Acid Colitis in Mice
Full text linkBackground/Aims: Compounds of Cannabis sativa are known to exert anti-inflammatory properties, some of them without inducing psychotropic side effects. Cannabidiol (CBD) is such a side effect-free phytocannabinoid that improves chemically induced colitis in rodents when given intraperitoneally. Here, we tested the possibility whether rectal and oral application of CBD would also ameliorate colonic inflammation, as these routes of application may represent a more appropriate way for delivering drugs in human colitis. Methods: Colitis was induced in CD1 mice by trinitrobenzene sulfonic acid. Individual groups were either treated with CBD intraperitoneally (10 mg/kg), orally (20 mg/kg) or intrarectally (20 mg/kg). Colitis was evaluated by macroscopic scoring, histopathology and the myeloperoxidase (MPO) assay. Results: Intraperitoneal treatment of mice with CBD led to improvement of colonic inflammation. Intrarectal treatment with CBD also led to a significant improvement of disease parameters and to a decrease in MPO activity while oral treatment, using the same dose as per rectum, had no ameliorating effect on colitis. Conclusion: The data of this study indicate that in addition to intraperitoneal application, intrarectal delivery of cannabinoids may represent a useful therapeutic administration route for the treatment of colonic inflammation. Copyright (C) 2012 S. Karger AG, Base
Nitric oxide as a mediator of bisacodyl and phenolphthalein laxative action: induction of nitric oxide synthase.
No full textSelective cannabinoid CB1 receptor-mediated inhibition of inducible nitric oxide synthase protein expression in C6 rat glioma cells.
No full textWe have studied the effects of two cannabinoid receptor agonists, WIN 55,212-2 and cannabinol, on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in the C6 glioma cell line. After 24 h of lipopolysaccharide (LPS) (1 mug/mL) and interferon-gamma (IFN-gamma) (300 U/mL) stimulation, a significant increase in NO production, evaluated as nitrite, was observed in the culture medium. WIN 55,212-2 (0.1 -10000 nm) and cannabinol (0.3-30000 nm), dose-dependently inhibited nitrite production showing a different potency (WIN 55,212-2 EC50: 4.2 nm; cannabinol EC50: 700 nm). WIN 55,212-2 (100 nm), given concomitantly to the stimulus also inhibited NOS expression but had no effect when added to the cells 2 h after LPS/IFN-gamma, indicating a possible interference at the protein synthesis level or at an earlier step, as gene transcription. The cannabinoid CB1 receptor antagonist, SR141716A (0.1-100 nm), but not the cannabinoid CB2 receptor antagonist, SR144528 (0.1-100 nm), reduced in a dose-related manner WIN 55,212-2-and cannabinol-induced inhibition of nitrite production. SR141161A also reversed the WIN 55,212-2-induced inhibition of NOS expression. These data suggest that selective cannabinoid CB1 receptor activation, by inhibiting NOS expression and NO overproduction in glial cells, might be helpful in NO-mediated inflammation leading to neurodegeneration
Modulation of peristalsis by cannabinoid CB(1) ligands in the isolated guinea-pig ileum
No full textThe effect of cannabinoid drugs on peristalsis in the guinea-pig ileum was studied. Peristalsis was induced by delivering fluid into the oral end of an isolated intestinal segment. Longitudinal muscle reflex contraction, threshold pressure and threshold volume to trigger peristalsis, compliance of the intestinal wall during the preparatory phase (a reflection of the resistance of the wall to distension) and maximal ejection pressure during the emptying phase of peristalsis were measured. The cannabinoid agonists WIN 55,212-2 (0.3 - 300 nM) and CP55,940 (0.3 - 300 nM) significantly decreased longitudinal muscle reflex contraction, compliance and maximal ejection pressure, while increased threshold pressure and volume to elicit peristalsis. These effects were not modified by the opioid antagonist naloxone (1 microM) and by the alpha-adrenoceptor antagonist phentolamine (1 microM). The inhibitory effect of both WIN 55,212-2 and CP55,940 on intestinal peristalsis was antagonized by the cannabinoid CB(1) receptor antagonist SR141716A (0.1 microM), but not by the cannabinoid CB(2) receptor antagonist SR144528 (0.1 microM). In absence of other drugs, the CB(1) receptor antagonists SR141716A (0.01 - 1 microM) and AM281 (0.01 - 1 microM) slightly (approximatively 20%) but significantly increased maximal ejection pressure during the empty phase of peristalsis without modifying longitudinal muscle reflex contraction, threshold pressure, threshold volume to trigger peristalsis and compliance. It is concluded that activation of CB(1) receptors reduces peristalsis efficiency in the isolated guinea-pig, and that the emptying phase of peristalsis could be tonically inhibited by the endogenous cannabinoid syste
Forgotten target for marijuana: the endocannabinoid system in the gut
No full textimpact factor 10.33
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