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Published on:November 2021
Indian Journal of Pharmaceutical Education and Research, 2021; 55(3s):S765-S773
Original Article | doi:10.5530/ijper.55.3s.183

The Effect of Taxifolin on Acrylamide-induced Oxidative and Proinflammatory Brain Injury in Rats: A Biochemical and Histopathological Study


Authors and affiliation (s):

Alevtina Ersoy1,*, Hasan Yasar1, Ceyda Tanoglu1, Gulce Naz Yazici2, Taha Abdulkadir Coban3, Yusuf Kemal Arslan4, Halis Suleyman5

1Department of Neurology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, TURKEY.

2Department of Histology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, TURKEY.

3Department of Biochemistry, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, TURKEY.

4Department of Biostatistics, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, TURKEY.

5Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, TURKEY.

Abstract:

Purpose: Acrylamide is a well-known environmental toxic compound. Taxifolin belongs to the group of flavonoids that have antioxidant, antimicrobial, anti-inflammatory and anticarcinogenic properties. In this study, we investigated the effect of taxifolin on acrylamiderelated oxidative and proinflammatory brain damage. Methods: The experimental animals were divided into three groups: (1) those treated with acrylamide 20 mg/kg p.o., (2) those treated with taxifolin 50 mg/kg p.o. and acrylamide and (3) the control group. At the end of the experiment, the rat brain tissues were examined for the levels of Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). A histopathological analysis was performed to detect the morphological changes in the brain. Results: Exposure to acrylamide caused a significant increase in the levels of MDA, TNF-α and IL-1β and a decrease in the values of tGSH, which indicates the presence of oxidative stress and inflammation in the brain tissue. Taxifolin treatment significantly reduced the levels of MDA and TNF-α and brought the mean values of IL-1β and tGSH close to those of the control group. The group that received acrylamide exhibited histopathological changes, such as neuronal degeneration, edema of microglia, dilated and congestive vessels and apoptotic inclusion. The use of taxifolin significantly improved the morphological changes in the brain tissue of the acrylamideexposed rats. Conclusion: Acrylamide causes brain damage, inducing oxidative stress and inflammation. Due to its antioxidant and anti-inflammatory properties, taxifolin may be one of the agents that can reduce the neurotoxic effects of acrylamide.

Key words: Acrylamide, Brain damage, Inflammation, Neurotoxicity, Oxidative stress, Taxifolin.

 




 

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The Official Journal of Association of Pharmaceutical Teachers of India (APTI)
(Registered under Registration of Societies Act XXI of 1860 No. 122 of 1966-1967, Lucknow)

Indian Journal of Pharmaceutical Education and Research (IJPER) [ISSN-0019-5464] is the official journal of Association of Pharmaceutical Teachers of India (APTI) and is being published since 1967.

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