The present study evaluated biochemical endpoints characterizing acrylamide (ACR) neurotoxicity in the cortex of rats, following the possible neuroprotective activity of thymoquinone (TQ), an active constituent of Nigella sativa. ACR (50 mg/kg, intraperitoneal [i.p.]) concurrently with TQ (2.5, 5 and 10 mg/kg, i.p.) for 11 days were administered to rats. As positive control, vitamin E was used. After 11 days of injections, narrow beam test (NBT) was performed. The levels of reduced glutathione (GSH) and malondialdehyde (MDA) were measured and Western blotting was done for mitogen-activated protein kinases (MAPKinases) and apoptosis pathways proteins in the rats' cortex. Additionally, Evans blue assay was done to evaluate the integrity of blood brain barrier (BBB). Administration of ACR significantly induced gait abnormalities. A significant decrease and increase in the levels of GSH and MDA was observed in the cortex of ACR-treated rats, respectively. The elevation in the levels of caspases 3 and 9, glial fibrillary acidic protein (GFAP) content, and Bax/Bcl-2, P-P38/P38 and P-JNK/JNK ratios accompanied by reduction in myelin basic protein (MBP) content and P-ERK/ERK ratio were noticed in the ACR group. TQ (5 mg/kg) improved gait abnormalities, and restored these changes. ACR affected the integrity of BBB while TQ was able to maintain the integrity of this barrier. TQ reversed the alterations in the protein contents of MAP kinase and apoptosis signaling pathways as well as MBP and GFAP contents, induced by ACR. It protected against ACR-mediated neurotoxicity, partly through its antioxidant and antiapoptotic properties.

中文翻译：

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氧化应激，MAPKinase和细胞凋亡途径在胸腺嘧啶对丙烯酰胺诱导的大鼠中枢神经系统毒性的保护作用中的作用。

本研究评估了在大鼠皮层中丙烯酰胺（ACR）的神经毒性的生化终点，随后观察到了可有效吸收Nigella sativa的活性成分胸腺醌（TQ）的神经保护作用。向大鼠施用ACR（50 mg / kg，腹膜内[ip]）与TQ（2.5、5和10 mg / kg，ip）并用11天。使用维生素E作为阳性对照。注射11天后，进行窄束测试（NBT）。测量了还原型谷胱甘肽（GSH）和丙二醛（MDA）的水平，并对大鼠皮质中的促分裂原活化蛋白激酶（MAPKinases）和凋亡通路蛋白进行了蛋白质印迹分析。此外，还进行了Evans蓝分析以评估血脑屏障（BBB）的完整性。施用ACR会明显导致步态异常。在ACR处理的大鼠皮层中分别观察到GSH和MDA含量显着降低和升高。半胱氨酸蛋白酶3和9，神经胶质纤维酸性蛋白（GFAP）含量以及Bax / Bcl-2，P-P38 / P38和P-JNK / JNK比值的升高伴随着髓磷脂碱性蛋白（MBP）含量的降低在ACR组中观察到P-ERK / ERK比。TQ（5 mg / kg）改善了步态异常，并恢复了这些变化。ACR影响了BBB的完整性，而TQ能够保持此屏障的完整性。TQ逆转了ACR诱导的MAP激酶和凋亡信号通路的蛋白质含量以及MBP和GFAP含量的改变。它部分地通过其抗氧化剂和抗凋亡特性来保护免受ACR介导的神经毒性。