Goudarzi Mehdi, Mombeini Mohammad Amin, Fatemi Iman, Aminzadeh Azadeh, Kalantari Heibatullah, Nesari Ali, Najafzadehvarzi Hossein, Mehrzadi Saeed
a Medicinal Plant Research Center , Ahvaz Jundishapur University of Medical Sciences , Ahvaz , Iran.
b Physiology-Pharmacology Research Center , Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences , Rafsanjan , Iran.
Neurol Res. 2019 May;41(5):419-428. doi: 10.1080/01616412.2019.1576319. Epub 2019 Feb 8.
Acrylamide (ACR) is an environmental contaminant and a well-known neurotoxin. Ellagic acid (EA), a natural plant polyphenol, has shown a variety of beneficial effects. The present study was designed to explore whether EA could attenuate ACR-induced neurotoxicity in rats and to explore the underlying mechanisms. Animals were divided into five groups. Group 1 was treated with normal saline (2 mL/kg) for 30 days. Group 2 was treated with ACR (20 mg/kg, orally) for 30 days. Groups 3 and 4 were treated with ACR and EA (10 and 30 mg/kg, orally) for 30 days. Group 5 was treated with EA (30 mg/kg, orally) for 30 days. Open field, rotarod and passive avoidance test were conducted to evaluate behavioral changes, respectively. The brain cortex was used for histological examination. Different oxidative parameters and inflammatory biomarkers were assessed in the brain cortex. ACR-administered rats showed a considerable impairment in exploratory behavior, motor performance as well as cognition. Our data also showed that ACR administration significantly increases malondialdehyde, nitric oxide, interleukin-1β and tumor necrosis factor-α levels. Moreover, it decreases brain glutathione level, superoxide dismutase, glutathione peroxidase, catalase activity. Co-administration of EA (especially 30 mg/kg, p.o.) prevented these changes; however, it did not affect the glutathione peroxidase activity. These results were supported by histopathological observations of the brain. Our results suggest that EA can be useful for protecting brain tissue against ACR-induced neurotoxicity through ameliorative effects on inflammatory indices and oxidative stress parameters.
丙烯酰胺（ACR）是一种环境污染物，也是一种知名的神经毒素。鞣花酸（EA）是一种天然植物多酚，已显示出多种有益作用。本研究旨在探讨EA是否能减轻ACR诱导的大鼠神经毒性，并探究其潜在机制。将动物分为五组。第1组用生理盐水（2 mL/kg）处理30天。第2组用ACR（20 mg/kg，口服）处理30天。第3组和第4组用ACR和EA（10和30 mg/kg，口服）处理30天。第5组用EA（30 mg/kg，口服）处理30天。分别进行旷场试验、转棒试验和被动回避试验以评估行为变化。取大脑皮层进行组织学检查。评估大脑皮层中不同的氧化参数和炎症生物标志物。给予ACR的大鼠在探索行为、运动表现以及认知方面表现出明显受损。我们的数据还表明，给予ACR会显著增加丙二醛、一氧化氮、白细胞介素-1β和肿瘤坏死因子-α水平。此外，它会降低大脑谷胱甘肽水平、超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶活性。联合给予EA（尤其是30 mg/kg，口服）可预防这些变化；然而，它不影响谷胱甘肽过氧化物酶活性。这些结果得到了大脑组织病理学观察的支持。我们的结果表明，EA通过改善炎症指标和氧化应激参数，可有效保护脑组织免受ACR诱导的神经毒性。
