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Oral Pretreatment (oral + pretreatment)
Selected AbstractsAntilipoperoxidative and antioxidant effects of S-allyl cysteine sulfoxide on isoproterenol-induced myocardial infarction in wistar ratsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 4 2006T. Sangeetha Abstract Our study evaluates the preventive effect of S-allyl cysteine sulfoxide (SACS) on lipid peroxidative products and enzymic and nonenzymic antioxidants in isoproterenol (ISO) induced myocardial infarction in rats. The male Wistar rats were rendered myocardial infarction by ISO (150 mg kg,1, once a day for two days). The concentrations of thiobarbituric acid reactive substances and lipid hydroperoxides were increased in hearts from ISO-treated rats, whereas the content of enzymic and nonenzymic antioxidants were declined in rats administered ISO. Oral pretreatment with SACS (40 mg kg,1 and 80 mg kg,1 daily for a period of 35 days) significantly (p < 0.05) decreased the lipid peroxidative products and significantly (p < 0.05) increased antioxidants in ISO-induced rats. Oral administration of SACS (40 mg kg,1 and 80 mg kg,1) did not show any significant effect in normal rats. Thus, the present study shows that SACS exhibits antilipoperoxidative and antioxidant effects in experimental myocardial infarction. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:167,173, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20132 [source] Inhibitors of the Na+/H+ Exchanger Cannot Prevent Atrial Electrical Remodeling in the GoatJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2004YURI BLAAUW M.D. Introduction: It has been suggested that blockade of the Na+/H+ exchanger (NHE1) can prevent atrial fibrillation (AF)-induced electrical remodeling and the development of AF. Methods and Results: AF was maintained by burst pacing in 10 chronically instrumented conscious goats. Intravenous and oral dosages of two NHE1 blockers (EMD87580 and EMD125021) resulted in plasma levels several magnitudes higher than required for effective NHE1 blockade. Shortening of atrial refractoriness immediately after 5 minutes of AF was not prevented by NHE1 blockade. In remodeled atria, increasing dosages of EMD87580 and EMD125021 did not reverse shortening of the atrial refractory period or reduce the duration of AF episodes. The cycle length during persistent AF also was not affected. Oral pretreatment with EMD87580 (8 mg/kg bid) starting 3 days before AF could not prevent electrical remodeling. After 24 and 48 hours of remodeling, the duration of AF paroxysms was 47 ± 32 seconds and 135 ± 63 seconds compared to 56 ± 17 seconds and 136 ± 52 seconds in placebo-treated animals (P > 0.8), respectively. Conclusion: In the goat model of AF, the Na+/H+ exchanger inhibitors EMD87580 and EMD125021 did not prevent or revert AF-induced electrical remodeling. This indicates that activation of the Na+/H+ exchanger is not involved in the intracellular pathways of electrical remodeling. This does not support the suggestion that blockers of the Na+/H+ exchanger may be beneficial for prevention and treatment of AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 440-446, April 2004) [source] Protective effect of glucosamine against ibuprofen-induced peptic ulcer in ratsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2007Sethumadhavan Santhosh Abstract Background:,Helicobacter pylori is the major causative factor of ulcer but the use of ibuprofen and other non-steroidal anti-inflammatory drugs have also been implicated in development of ulcer. The purpose of the present study was to determine the anti-ulcer effect of glucosamine. Methods:, The protective effect of glucosamine on ibuprofen-induced peptic ulcer in male albino rats was studied with respect to changes in the volume of gastric juice, acid output, pepsin activity, activities of membrane bound ATPases, protein content, glycoprotein components and histopathology. Results:, Oral administration of ibuprofen caused significant increase in the number of lesions in the gastric mucosa, increases in the volume of gastric juice and acidity, and decreased activity of pepsin. The levels of protein content and glycoprotein components (hexose, hexosamine and sialic acid) and ATPase activities were also observed. Oral pretreatment with glucosamine resulted in significant reduction in the number of lesions in the gastric mucosa and decreases in the volume of gastric juice and acidity. The pepsin activity was also maintained at near normalcy. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced depletion of protein and glycoprotein components and maintained the activities of membrane bound ATPases as compared to untreated ulcer induced group of rats. Conclusion:, The anti-ulcerogenic activity of glucosamine might be ascribable to its ability to neutralize the hydrochloric acid secreted into the stomach and to its capability to strengthen the mucosal barrier by increasing mucosal glycoprotein synthesis and to its free radical scavenging property. Histopathological investigations of the mucosal tissue also support the anti-ulcerogenic effect of glucosamine. [source] The antiulcer activity of Garcinia cambogia extract against indomethacin-induced gastric ulcer in ratsPHYTOTHERAPY RESEARCH, Issue 1 2002P. Mahendran Abstract Garcinia cambogia extract is a herbal preparation that has been suggested as useful in the treatment of gastrointestinal disorders. In the present study this drug was tested for its antiulcerogenic effect. Oral pretreatment with Garcinia cambogia fruit extract (1,g/kg body wt/day) for 5, 10 or 15 days protected the gastric mucosa against the damage induced by indomethacin (20,mg/kg body wt). The volume and acidity of the gastric juice decreased in the pretreated rats. The glycoprotein levels of the gastric contents which were decreased in the untreated rats, maintained near normal levels in the pretreated rats. Protein which was elevated in the gastric juice of untreated rats, showed near normal levels in the pretreated rats. Garcinia cambogia was able to decrease the acidity and to increase the mucosal defence in the gastric areas, thereby justifying its use as an antiulcerogenic agent. Copyright © 2002 John Wiley & Sons, Ltd. [source] s -CARBOXYMETHYLCYSTEINE INHIBITS CARBACHOL-INDUCED CONSTRICTION OF EPITHELIUM-DENUDED RAT AND HUMAN AIRWAY PREPARATIONSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2008Dragan Pavlovic SUMMARY 1The effects of s-carboxymethyl-l-cysteine (S-CMC), either administered orally to rats or incubated with tissue preparations from rats and humans, on isometric contractions of tracheal smooth muscle were investigated in the present study using an improved in vitro model of tracheal tube or ring preparations. The involvement of the tracheal epithelium in the observed effects was also investigated. 2The experimental model permitted selective perfusion of the airway tube, luminal-IN or serosal,OUT, and measurement of airway smooth muscle contraction or relaxation in preparations with (+) or without (,) epithelium (Ep), excluding direct effects of airway mucus. 3We found that oral pretreatment of rats with S-CMC (mixed with water; 200 mg/kg per day for 2 weeks), but not short pre-incubation of preparations in vitro (10,3 mol/L S-CMC for 1 h), diminished the sensitivity of ,Ep preparations to carbachol compared with controls (EC50 (,log10 mol/L) values: 5.5 ± 0.1 vs 5.8 ± 0.1, respectively, for IN perfusion (P < 0.005); 5.6 ± 0.1 vs 5.9 ± 0.1, respectively, for OUT perfusion (P < 0.005)), whereas the sensitivity of preparations to aminophylline was not affected. Normal sensitivity to carbachol stimulation was re-established if preparations were pre-incubated with capsaicin. 4It was also found that longer pre-incubation (4 h) of ring-preparations of human bronchus with S-CMC (10,5 mol/L) in vitro resulted in a diminished response to carbachol stimulation. 5In conclusion, S-CMC had small inhibitory effects on the sensitivity of rat and human airway smooth muscle to carbachol, particularly in endothelium-denuded preparations. Whether the epithelium was responding to S-CMC by producing some contracting factor(s) requires further investigation. [source] | ||||||||||