Department of Internal Medicine, College of Medicine, Taif University, Taif, Saudi Arabia.
Physiology Department, National Organization for Drug Control and Research (NODCAR), Giza, 12553, Egypt.
Metab Brain Dis. 2018 Aug;33(4):1121-1130. doi: 10.1007/s11011-018-0222-6. Epub 2018 Mar 20.
Due to the high ability of cadmium to cross the blood-brain barrier, cadmium (Cd) causes severe neurological damages. Hence, the purpose of this study was to investigate the possible protective effect of Mangifera indica leaf extract (MLE) against Cd-induced neurotoxicity. Rats were divided into eight groups. Group 1 served as vehicle control group, groups 2, 3 and 4 received MLE (100, 200, 300 mg /kg b.wt, respectively). Group 5 was treated with CdCl (5 mg/kg b.wt). Groups 6, 7 and 8 were co-treated with MLE and CdCl using the same doses. All treatments were orally administered for 28 days. Cortical oxidative stress biomarkers [Malondialdehyde (MDA), nitric oxide (NO), glutathione content (GSH), oxidized form of glutathione (GSSG), 8-hydroxy-2-deoxyguanosine (8-OHdG), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)], inflammatory cytokines [tumor necrosis factor (TNF-α) and interlukin-1β (IL-1β)], biogenic amines [norepinephrine (NE), dopamine (DA) and serotonin (5-HT)], some biogenic metabolites [3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA)], acetylcholine esterase activity (AChE) and purinergic compound [adenosine triphosphate (ATP)] were determined in frontal cortex of rats. Results indicated that Cd increased levels of the oxidative biomarkers (MDA, NO, GSSG and 8-OHdG) and the inflammatory mediators (TNF-α and IL-1β), while lowered GSH, SOD, CAT, GPx and ATP levels. Also, Cd significantly decreased the AChE activity and the tested biogenic amines while elevated the tested metabolites in the frontal cortex. Levels of all disrupted cortical parameters were alleviated by MLE co-administration. The MLE induced apparent protective effect on Cd-induced neurotoxicity in concern with its medium and higher doses which may be due to its antioxidant and anti-inflammatory activities.
由于镉具有很强的穿透血脑屏障的能力,因此镉(Cd)会对神经系统造成严重损害。因此,本研究旨在探讨芒果叶提取物(MLE)对 Cd 诱导的神经毒性的可能保护作用。将大鼠分为八组。第 1 组作为载体对照组,第 2、3 和 4 组分别给予 MLE(100、200 和 300mg/kg bw)。第 5 组用 CdCl 治疗(5mg/kg bw)。第 6、7 和 8 组用相同剂量的 MLE 和 CdCl 共同处理。所有治疗均口服 28 天。皮质氧化应激生物标志物[丙二醛(MDA)、一氧化氮(NO)、谷胱甘肽含量(GSH)、氧化型谷胱甘肽(GSSG)、8-羟基-2-脱氧鸟苷(8-OHdG)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)]、炎性细胞因子[肿瘤坏死因子(TNF-α)和白细胞介素-1β(IL-1β)]、生物胺[去甲肾上腺素(NE)、多巴胺(DA)和 5-羟色胺(5-HT)]、一些生物代谢物[3,4-二羟基苯乙酸(DOPAC)、高香草酸(HVA)和 5-羟吲哚乙酸(5-HIAA)]、乙酰胆碱酯酶活性(AChE)和嘌呤化合物[三磷酸腺苷(ATP)]在大鼠前额皮质中进行了测定。结果表明,Cd 增加了氧化生物标志物(MDA、NO、GSSG 和 8-OHdG)和炎性介质(TNF-α和 IL-1β)的水平,同时降低了 GSH、SOD、CAT、GPx 和 ATP 的水平。此外,Cd 显著降低了前额皮质中 AChE 活性和测试生物胺的水平,同时升高了测试代谢物的水平。MLE 联合给药缓解了所有皮质参数的破坏。MLE 对 Cd 诱导的神经毒性具有明显的保护作用,这与其中高剂量有关,这可能与其抗氧化和抗炎活性有关。