l-carnitine (LC) plays an important role in the oxidative/antioxidative balance of different organs. The study has explored the effect of the daily administration of aspartame (ASP) at two different doses for 4 weeks induces oxidative stress, inflammation, and histopathology in the brain of rats. This study also focused on explaining whether l-carnitine (LC) has potential ameliorative effects against pathophysiology induced by ASP in the brain. Adult male Wistar rats were split into six groups as follows: control animals were administered with vehicle, group of ASP at a low dose (ASP-LD) was given 75 mg/kg B.W., high dose of ASP (ASP-HD; 150 mg/kg), animals were treated with LC (10 mg/kg), ASP-LD + LC group and ASP-HD + LC treated rats. ASP induced large increments in cytokines of interleukin-6, tumor necrosis factor-α, myeloperoxidase, xanthine oxidase, cyclooxygenase-2, and prostaglandin E2 in a dose-dependent response of the brain. Activities of superoxide dismutase/catalase, glutathione peroxidase, and acetylcholinesterase, besides levels of thiol, glutathione, a brain-derived neurotrophic factor, and neurotransmitters, were decreased in the brain tissue. The inauguration of brain injury by ASP administration was depended on the dose of treatment. Co-administration of LC with ASP significantly reversed and corrected all the abovementioned parameters. The data confirm that LC attenuated ASP neurotoxicity by suppressing the inflammation, oxidative stress and improving the neurotransmitters, antioxidants coupled with the histological and cellular structure.

中文翻译：

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左旋肉碱作为 Wistar 白化大鼠阿斯巴甜损伤的神经保护剂

左旋肉碱 (LC) 在不同器官的氧化/抗氧化平衡中起着重要作用。该研究探讨了每天服用两种不同剂量的阿斯巴甜 (ASP) 持续 4 周对大鼠大脑中氧化应激、炎症和组织病理学的影响。该研究还重点解释了左旋肉碱 (LC) 是否对大脑中由 ASP 诱导的病理生理学具有潜在的改善作用。成年雄性 Wistar 大鼠分为以下六组：对照动物给予载体，给予低剂量 ASP 组 (ASP-LD) 75 mg/kg BW，高剂量 ASP (ASP-HD; 150 mg /kg)，动物用 LC (10 mg/kg)、ASP-LD + LC 组和 ASP-HD + LC 治疗的大鼠进行治疗。ASP 诱导白细胞介素 6、肿瘤坏死因子 α、髓过氧化物酶、黄嘌呤氧化酶、环氧合酶-2 和前列腺素 E2 在大脑的剂量依赖性反应中。除了硫醇、谷胱甘肽、脑源性神经营养因子和神经递质的水平外，脑组织中的超氧化物歧化酶/过氧化氢酶、谷胱甘肽过氧化物酶和乙酰胆碱酯酶的活性也降低。ASP 给药对脑损伤的开始取决于治疗剂量。LC 与 ASP 的共同给药显着逆转并纠正了所有上述参数。数据证实，LC 通过抑制炎症、氧化应激和改善神经递质、抗氧化剂以及组织学和细胞结构来减弱 ASP 的神经毒性。除了硫醇、谷胱甘肽、脑源性神经营养因子和神经递质的水平外，脑组织中的超氧化物歧化酶/过氧化氢酶、谷胱甘肽过氧化物酶和乙酰胆碱酯酶的活性也降低。ASP 给药对脑损伤的开始取决于治疗剂量。LC 与 ASP 的共同给药显着逆转并纠正了所有上述参数。数据证实，LC 通过抑制炎症、氧化应激和改善神经递质、抗氧化剂以及组织学和细胞结构来减弱 ASP 的神经毒性。除了硫醇、谷胱甘肽、脑源性神经营养因子和神经递质的水平外，脑组织中的超氧化物歧化酶/过氧化氢酶、谷胱甘肽过氧化物酶和乙酰胆碱酯酶的活性也降低。ASP 给药对脑损伤的开始取决于治疗剂量。LC 与 ASP 的共同给药显着逆转并纠正了所有上述参数。数据证实，LC 通过抑制炎症、氧化应激和改善神经递质、抗氧化剂以及组织学和细胞结构来减弱 ASP 的神经毒性。ASP 给药对脑损伤的开始取决于治疗剂量。LC 与 ASP 的共同给药显着逆转并纠正了所有上述参数。数据证实，LC 通过抑制炎症、氧化应激和改善神经递质、抗氧化剂以及组织学和细胞结构来减弱 ASP 的神经毒性。ASP 给药对脑损伤的开始取决于治疗剂量。LC 与 ASP 的共同给药显着逆转并纠正了所有上述参数。数据证实，LC 通过抑制炎症、氧化应激和改善神经递质、抗氧化剂以及组织学和细胞结构来减弱 ASP 的神经毒性。