Abstract
Purpose: To examine the effect of taxifolin on I/R induced gastric injury in rats using biochemical and histopatholohical methods. Methods: Eighteen albino Wistar male rats equally grouped as; gastric I/R (I/R), 50 mg/kg taxifolin + gastric I/R (TAX+ I/R) and sham operation applied (SHAM). Ischemia induced for 1 hour, and reperfusion induced for 3 hours. Results: Oxidant parameters like, Malondialdehyde (MDA) and Hydroxyguanine (8-OHdG) were higher, whereas total glutathione (tGSH) was lower in the I/R group according to SHAM group, histopathological findings such as marked destruction, edema, and proliferated dilated congested blood vessels were observed severely in the I/R group, whereas there was not any pathological finding except mild dilated congested blood vessels in the TAX+ I/R group. Conclusion: The taxifolin can be clinically beneficial in the treatment of gastric injury due to I/R procedure.
Highlights
Ischemia, as is known, is defined as oxygen deprivation in tissues as a result of the decrease or whole cessation of blood flow to living tissues
Taxifolin administration decreased this elevation observed in the I/R group (p< 0.001)
Our results showed that I/R procedure significantly increased MDA level in gastric tissue compared to sham operation applied (SHAM) and taxifolin group
Summary
As is known, is defined as oxygen deprivation in tissues as a result of the decrease or whole cessation of blood flow to living tissues. Reoxygenation in reperfusion results in xanthine oxidase, which is formed and accumulated during ischemia, to react with molecular oxygen and form excess free oxygen radicals[1]. Parks et al.[2] showed that reperfusion injury caused much more damage than ischemia alone due to this mechanism. Over-produced free oxygen radicals oxidize the lipids of cell membranes to produce toxic substances like malondialdehyde (MDA) from lipids. Free radicals react with DNA to cause oxidative damage in the DNA. The roles of increase in MDA production and decrease in total glutathione (tGSH) production have been shown in the pathogenesis of gastric ischemia-reperfusion (I/R) injury[4]. Polat et al.[5] reported that 8-OHGua was increased in parallel with the increase of gastric oxidative damage. It was thought that drugs that inhibits the overproduction of MDA and excessive consumption of tGSH may be usefull in the treatment of gastric I/R
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
