Department of Pharmacology and Toxicology, Pharmacy College, King Saud University, Riyadh, Saudi Arabia.
J Biochem Mol Toxicol. 2020 Apr;34(4):e22449. doi: 10.1002/jbt.22449. Epub 2020 Jan 22.
Propionic acid (PRA) is used as a food preservative. This study was aimed to investigate the neuroprotective effect of acetyl-l-carnitine (ALC) and nano-Coenzyme Q (N-CoQ) on brain intoxication induced by PRA in rats. Rats were divided into five groups: group I: control; group II: received PRA; group III: received ALC; group IV: received N-CoQ; and group V: received ALC and N-CoQ for 5 days. The antioxidants in question markedly ameliorated serum interleukin-1β and tumor necrosis factor-α, and brain NO, lipid peroxide, glutathione, and superoxide dismutase levels as well as protein expression of brain-derived neurotrophic factor (BDNF) and P-cyclic-AMP response element-binding protein (CREB) that were altered by a toxic dose of PRA, as well as histopathological alterations, including improvement of the cerebellum architecture. Interestingly, the combination therapy of ALC and N-CoQ achieved the most neuroprotective effect compared with monotherapies. The current study established that N-CoQ is considered as a useful tool to prevent brain injury induced by PRA. BDNF and CREB proteins are involved in both PRA neurotoxicity and treatment.
丙酸(PRA)被用作食品防腐剂。本研究旨在探讨乙酰左旋肉碱(ALC)和纳米辅酶 Q(N-CoQ)对 PRA 诱导的大鼠脑中毒的神经保护作用。大鼠分为五组:I 组:对照组;II 组:给予 PRA;III 组:给予 ALC;IV 组:给予 N-CoQ;V 组:给予 ALC 和 N-CoQ 连续 5 天。这些抗氧化剂显著改善了血清白细胞介素-1β和肿瘤坏死因子-α以及大脑 NO、脂质过氧化物、谷胱甘肽和超氧化物歧化酶水平以及脑源性神经营养因子(BDNF)和 cAMP 反应元件结合蛋白(CREB)的蛋白表达,这些改变是由 PRA 的毒性剂量引起的,以及包括改善小脑结构在内的组织病理学改变。有趣的是,与单药治疗相比,ALC 和 N-CoQ 的联合治疗取得了最有效的神经保护作用。本研究确立了 N-CoQ 被认为是预防 PRA 诱导的脑损伤的有用工具。BDNF 和 CREB 蛋白均参与 PRA 神经毒性和治疗。