Protective Effect of Green Tea Aqueous Extract on Acrylamide Induced Neurotoxicity

被引:16
|
作者
Esmaeelpanah, Elahe [1 ]
Rahmatkhah, Alireza [1 ]
Poormahmood, Narges [1 ]
Razavi, Bibi Marjan [2 ]
Hasani, Faezeh Vandati [1 ]
Hosseinzadeh, Hossein [3 ]
机构
[1] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Iran
[2] Mashhad Univ Med Sci, Targeted Drug Delivery Res Ctr, Dept Pharmacodynamy & Toxicol, Sch Pharm, Mashhad, Iran
[3] Mashhad Univ Med Sci, Pharmaceut Res Ctr, Dept Pharmacodynamy & Toxicol, Sch Pharm, Mashhad, Iran
关键词
Green Tea; Acrylamide; Camellia Sineasis; Neu rotoxicity Syndromes;
D O I
10.17795/jjnpp-18406
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: Acrylamide (ACR) monomer is an effective neurotoxicant, which damages the central and peripheral nervous systems in humans and animals. Green tea, an infusion from the leaves of Camellia sinensis Theaceae, is a known antioxidant traditional medicine. Objectives: In this study the protective effect of green tea aqueous extract (GTAE) was evaluated on ACR induced neurotoxicity. Materials and Methods: In our in vitro study, the effect of different concentrations of GTAE on ACR toxicity (IC50) in PC12 cells was evaluated using MIT assay. Moreover in another experiment, the effect of GTAE on neural toxicity induced by ACR was evaluated in rats. Results: Treatment with ACR (50 mg/kg via intraperitoneal injection for 11 days), induced severe gait abnormalities and significantly decreased body weight at the end of 11 days. Treatment with GTAE (6.25, 12.5, 25 and 50 mg/kg) reduced ACR-induced neurotoxicity, but the effect was only significant in a group which received GTAE at a dose of 12.5 mg/kg and ACR(P < 0.01). ACR decreased cell viability in PC12 cells used as an in vitro model. Pretreatment with GTAE (7.8. 62.5 mu g/mL) decreased ACR-induced cytotoxicity(P < 0.01 and P < 0.001, respectively). Conclusions: As green tea is an essential source of antioxidants such as flavonoids, suppression of reactive oxygen species (ROS) generation may be in part considered as the neuroprotective mechanism on ACR induced neurotoxicity.
引用
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页码:1 / 5
页数:5
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