Abstract
The activity of dexamethasone and taxifolin {(2R, 3R)-2-(3, 4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one}supplementation on prostaglandin E2 and thromboxane A2 in gastric acid secretion and anti-ulcer was studied. Twenty male Wistar rats (180g-200g body weight) were used. The rats were randomly selected into four groups containing 5 rats each. Group 1 was the control group fed on normal rat feed. Group 2 received 3mg/kg of Dexamethasone (intraperitoneally) at one day interval. Group 3 received 3mg/kg of Dex. intraperitoneally and 1mg/kg body weight of taxifolin orally while group 4 received 1mg/kg body weight of taxifolin. At the end of 6 weeks, basal and peak gastric acid output was measured by continuous perfusion of rats stomach under anaesthesia with normal saline at the rate of 1ml/min. Gastric acid, mucus secretion, ulcer index, PGE-2 and thromboxane A2 activity were determined according to standard procedures. Results showed a significantly (p<.05) decreased prostaglandin and mucus secretion level and a raised thromboxane concentrations and gastric acid output in dexamethasone administration. Taxifolin significantly (p<.05) lowered thromboxane A2 concentration in Dex treatment while increasing the prostaglandin E2 level. We conclude that Taxifolin decreases dexamethasone- induced gastric acid secretion, increases prostaglandin activity but reduces thromboxane concentration.
Highlights
Dexamethasone is a synthetic glucocorticoid that appears to have a double face effect
Its activity in man and experimental animals has generated a long standing debate on whether treatment with glucocorticoids leads to peptic ulcer or not [1,2] Available reports have shown that the use of glucocorticoids could be gastroprotective under physiologic conditions [3] on one hand, and on the other hand, could be causal to many disease states such as hypertension associated with increased oxidative stress and excess production of reactive oxygen species (ROS) often generated by nicotinamide adenine dinucleotide phosphate-oxidase (NAPDH) [4] and contributing to tissue damage, nitric oxide (NO) deficiency and endothelial dysfunction
Basal gastric acid secretion and maximal (Histamine -induced), prostaglandin E2 and thromboxane A2 activity were determined according to standard procedures
Summary
Dexamethasone is a synthetic glucocorticoid that appears to have a double face effect. Various works have demonstrated that the administration of glucocorticoids to animals can attenuate gastric mucosal erosion formation [6,7, 8]. It has been shown that pretreatment with dexamethasone [6, 7] may protect the stomach from ethanol or non-steroidal anti-inflammatory drugs (NSAID)-induced injury, respectively thereby maintaining the gastric mucosal integrity [9, 10]. Corresponding author: Etah Etah Nkanu Department of Physiology, Faculty of Basic Medical Sciences, Cross River University of Technology, Calabar, Okuku Campus, Yala, Nigeria.
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