Therapeutic role of quercetin on oxidative damage induced by acrylamide in rat brain

被引:24
作者
Zargar, Seema [1 ]
Siddiqi, Nikhat Jamal [1 ]
Ansar, Sabah [2 ]
Alsulaimani, Maha Saleh [1 ]
El Ansary, Afaf K. [1 ]
机构
[1] King Saud Univ, Dept Biochem, Coll Sci, Riyadh 11495, Saudi Arabia
[2] King Saud Univ, Dept Clin Sci, Coll Appl Med Sci, Riyadh, Saudi Arabia
关键词
Dopamine; interferon-alpha; oxidative stress; neurotransmitters; neurotoxicity; CADMIUM FLUORIDE; IDENTIFICATION; NEUROTOXICITY; FORMALDEHYDE; STRESS; LIVER;
D O I
10.3109/13880209.2015.1127977
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context Quercetin (QE), a bioflavonoid present abundantly in fruits and vegetables, has been reported to possess antioxidant properties. Acrylamide (ACR) is formed in foods during cooking and is known to be neurotoxic.Objective The present study was designed to evaluate the protective effect of QE against neurotoxicity induced by ACR.Materials and methods Four groups of Wistar rats consisting of six rats each: (i) control group; (ii) acrylamide treated group (50mg/kg body weight as single dose); (iii) quercetin group: rats were treated intraperitoneally (i.p.) with QE (10mg/kg body weight alone every day for 5 d); (iv) quercetin+acrylamide group: quercetin (10mg/kg bw) was given i.p. every day for 5 d followed by acrylamide i.p. injection (50mg/kg bw) on fifth day (single dose). Rats were killed after 48h.Results Administration of ACR (50mg/kg bw) in Wistar rats resulted in significant increase of dopamine, interferon- and 8-hydroxyguanosine with concomitant decrease of serotonin (p<0.001) in the rat brain. Treatment of rats with QE intraperitonealy (10mg/kg body weight) before ACR assault resulted in the diminution of ACR-mediated neurotoxicity as evident from decreased levels of dopamine, interferon- (p<0.001) and 8-hydroxyguanosine with concomitant restoration of serotonin levels (p<0.001).Discussion and conclusion On the basis of the above results, the present study suggests that quercetin may be a potential therapeutic agent for restoration of oxidative damage to neurons.
引用
收藏
页码:1763 / 1767
页数:5
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