Asejeje Folake Olubukola, Abiola Michael Abayomi, Adeyemo Oluwatobi Adewumi, Ogunro Olalekan Bukunmi
Department of Chemical Sciences, Faculty of Natural Sciences, Ajayi Crowther University, Oyo, Nigeria.
Department of Chemical Sciences, Faculty of Natural Sciences, Ajayi Crowther University, Oyo, Nigeria.
Toxicol Lett. 2025 Jul;410:121-129. doi: 10.1016/j.toxlet.2025.06.008. Epub 2025 Jun 7.
Sodium benzoate (SB) is a commonly utilized food preservative in the food business. Nonetheless, apprehensions regarding its impact on the brain have garnered worldwide attention. Consequently, we examined the effect of SB on lipopolysaccharide (LPS)-induced neurotoxicity in rats. Twenty-eight male Wistar rats were randomly assigned to four groups: Group 1 (Control, distilled water), Group 2 (SB, 600 mg/kg), Group 3 (LPS, 250 μg/kg/day), and Group 4 (LPS + SB; LPS, 250 μg/kg + SB, 600 mg/kg). SB was administered orally for 14 days, whereas LPS was injected intraperitoneally for 7 days. Upon completion of the treatment, locomotor, motor, and exploratory behaviors were assessed, followed by biochemical, molecular, and histological analyses of the rat brain. Results indicated that SB exacerbated LPS-induced impairments in exploratory behavior and locomotion in rats. Furthermore, SB intensified LPS-induced oxidative stress and cholinergic impairment, as evidenced by reduced levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione-S-transferase (GST) activity, alongside an increase in malondialdehyde (MDA) and acetylcholinesterase (AChE) activity in brain tissue. Similarly, exposure to SB led to a substantial elevation in the levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), as well as nitric oxide (NO) and myeloperoxidase (MPO) activity in the rat brain. Additionally, histological examination reveals degenerative neurons in the cerebellum, cortex, and hippocampus CA1 and CA3 areas. The outcomes of this study indicate that the co-administration of SB with LPS exacerbated the neurotoxic damage caused by LPS in the rat brain.
苯甲酸钠（SB）是食品行业中常用的食品防腐剂。尽管如此，对其对大脑影响的担忧已引起全球关注。因此，我们研究了SB对大鼠脂多糖（LPS）诱导的神经毒性的影响。28只雄性Wistar大鼠被随机分为四组：第1组（对照组，蒸馏水），第2组（SB组，600mg/kg），第3组（LPS组，250μg/kg/天），第4组（LPS+SB组；LPS，250μg/kg+SB，600mg/kg）。SB口服给药14天，而LPS腹腔注射7天。治疗结束后，评估运动、运动和探索行为，随后对大鼠大脑进行生化、分子和组织学分析。结果表明，SB加剧了LPS诱导的大鼠探索行为和运动障碍。此外，SB加剧了LPS诱导的氧化应激和胆碱能损伤，脑组织中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）水平降低以及谷胱甘肽-S-转移酶（GST）活性降低，同时丙二醛（MDA）和乙酰胆碱酯酶（AChE）活性增加证明了这一点。同样，暴露于SB导致大鼠大脑中促炎细胞因子水平大幅升高，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6），以及一氧化氮（NO）和髓过氧化物酶（MPO）活性。此外，组织学检查显示小脑、皮层以及海马CA1和CA3区域存在神经元变性。本研究结果表明，SB与LPS共同给药加剧了LPS对大鼠大脑造成的神经毒性损伤。
