Research Article: Effect of taxifolin on oxidative gastric injury induced by celiac artery ligation in rats1

Date Published: May 06, 2019

Publisher: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia

Author(s): Hüseyin Eken, Orhan Cimen, Ferda Keskin Cimen, Eray Kurnaz, Murat Yildirim, Volkan Tasova, Nezahat Kurt, Kamil Pehlivanoglu, Didem Onk, Asli Ozbek Bilgin.

http://doi.org/10.1590/s0102-865020190040000004

Abstract

To examine the effect of taxifolin on I/R induced gastric injury in rats using biochemical and histopatholohical 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.

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.

The taxifolin can be clinically beneficial in the treatment of gastric injury due to I/R procedure.

Partial Text

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. Reperfusion is the process of blood build up in ischemic tissue. However, reoxygenation in reperfusion results in xanthine oxidase, which is formed and accumulated during ischemia, to react with molecular oxygen and form excess free oxygen radicals1. 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. Also, free radicals react with DNA to cause oxidative damage in the DNA. One of the product of oxidative DNA damage is 8 hydroxyguanine (8-OHGua) and is used as an important parameter in determining oxidative stress3. In recent studies, 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) injury4. Polat et al.5 also reported that 8-OHGua was increased in parallel with the increase of gastric oxidative damage. Therefore, 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.

Animal experiments were performed according to the National Guidelines for the Use and Care of Laboratory Animals and were confirmed by the local animal ethics committee of Atatürk University, Erzurum, Turkey (Ethics Committee Number: 75296309-050.01.04-E.1800138966, Dated:04.05.2018).

As is known, gastric I/R damage can occur in the resection process and other pathological conditions (shock, burns, trauma, vascular rupture), and cause multiple organ failure which is a reason of death6-8. Hence, research on the treatment of gastric injury and fatal complications due to I/R procedure is ongoing. In this experimental study, biochemical and histopathological effects of taxifolin on gastric I/R injury were investigated in rats. Biochemical parameters such as MDA, 8-OHdG and tGSH were used to evaluate the protective effect of taxifolin towards gastric I/R injury. It was also investigated whether the changes in MDA, tGSH and 8-OHdG levels were reflected in histopathological findings. Our results showed that I/R procedure significantly increased MDA level in gastric tissue compared to SHAM and taxifolin group. Our previous experimental study also presented that I/R procedure elevated MDA level in animal gastric tissue4. As it is known, MDA is last molecule of lipid peroxidation (LPO), also a good marker to evaluate oxidative tissue damage21. LPO is induced by free oxygen radicals (ROS). In liver tissues, ROS is produced by xanthine oxidase accumulated during the ischemic period reacting with the abundant molecular oxygen introduced to the tissue during reperfusion1. MDA was offered to be increased in I/R and different gastric injury models in many previous and recent studies22. This implies that our results are consistent with the literature.

The I/R process changed the oxidant antioxidant balance in the gastric tissue of the animals in favor of the oxidants.This indicates that the I/R process causes oxidative damage in gastric tissue of animals. Taxifolin changed the oxidant antioxidant balance to favor to oxidants in the I/R applied anima and suppressed the I/R related oxidative gastric damage . Also suppressing the elevation of oxidant parameters and reduction of antioxidant parameters, taxifolin significantly minimized the histopathologic damage induced by I/R in the gastric tissue. These findings suggest that taxifolin can be clinically beneficial in the treatment of gastric injury due to I/R procedure.

 

Source:

http://doi.org/10.1590/s0102-865020190040000004

 

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