Hassanen Eman I, Issa Marwa Y, Hassan Neven H, Ibrahim Marwa A, Fawzy Iten M, Fahmy Sherif Ashraf, Mehanna Sally
Department of Pathology, Faculty of Veterinary Medicine, Cairo University, 12211 Giza, Egypt.
Department of Pharmacognosy, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, 11562 Cairo, Egypt.
ACS Omega. 2023 May 17;8(21):18491-18508. doi: 10.1021/acsomega.2c08295. eCollection 2023 May 30.
Imidacloprid (IMI) insecticide is rapidly metabolized in mammals and contributes to neurotoxicity via the blocking of nicotinic acetylcholine receptors, as in insects. retains its great antioxidant potential in both fresh and dry forms. No data is available on the neuroprotective effect of this plant in laboratory animals. In this context, aerial parts of were used to prepare the essential oil (OMO) and methanol extract (OME). The potential neuroprotective impact of both OMO and OME against IMI-induced neurotoxicity in rats was explored. Forty-two rats were divided into 6 groups, with 7 rats in each one. Rats were daily administered the oral treatments: normal saline, OMO, OME, IMI, IMI + OMO, and IMI + OME. Our results revealed the identification of 55 components in essential oil, most belonging to the oxygenated and hydrocarbon monoterpenoid group. Moreover, 37 constituents were identified in the methanol extract, mostly phenolics. The potent neurotoxic effect of IMI on rats was confirmed by neurobehavioral and neuropathological alterations and a reduction of both acetylcholine esterase (AchE) activity and dopamine (DA), serotonin (5HT), and γ-aminobutyric acid (GABA) levels in the brain. Exposure of rats to IMI elevates the malondialdehyde (MDA) levels and reduces the antioxidant capacity. IMI could upregulate the transcription levels of nuclear factor-κB (NF-κB), interleukin-1 β (IL-1β), and tumor necrosis factor (TNF-α) genes and express strong caspase-3 and inducible nitric oxide synthase (iNOS) immunostaining in most examined brain areas. On the other hand, rats coadministered OMO or OME with IMI showed a marked improvement in all of the studied toxicological parameters. In conclusion, cotreatment of extracts with IMI can protect against IMI neurotoxicity via their potent antioxidant, anti-inflammatory, and anti-apoptotic effects. Thus, we recommend a daily intake of to protect against insecticide's oxidative stress-mediated neuroinflammatory stress and apoptosis. The molecular docking study of linalool, rosmarinic acid, γ-terpene, and terpene-4-ol justify the observed normalization of the elevated iNOS and TNF-α levels induced after exposure to IMI.
吡虫啉（IMI）杀虫剂在哺乳动物体内迅速代谢，并像在昆虫体内一样，通过阻断烟碱型乙酰胆碱受体而导致神经毒性。[植物名称]无论是新鲜形式还是干燥形式都具有很强的抗氧化潜力。关于这种植物对实验动物的神经保护作用尚无数据。在此背景下，[植物名称]的地上部分被用于制备精油（OMO）和甲醇提取物（OME）。研究了OMO和OME对大鼠IMI诱导的神经毒性的潜在神经保护作用。42只大鼠分为6组，每组7只。大鼠每天接受口服处理：生理盐水、OMO、OME、IMI、IMI + OMO和IMI + OME。我们的结果显示在[植物名称]精油中鉴定出55种成分，大多数属于氧化型和烃类单萜类。此外，在甲醇提取物中鉴定出37种成分，主要是酚类。IMI对大鼠的强烈神经毒性作用通过神经行为和神经病理学改变以及脑中乙酰胆碱酯酶（AchE）活性和多巴胺（DA）、5-羟色胺（5HT）和γ-氨基丁酸（GABA）水平的降低得到证实。大鼠接触IMI会提高丙二醛（MDA）水平并降低抗氧化能力。IMI可上调核因子-κB（NF-κB）、白细胞介素-1β（IL-1β）和肿瘤坏死因子（TNF-α）基因的转录水平，并在大多数检测的脑区中表现出强烈的半胱天冬酶-3和诱导型一氧化氮合酶（iNOS）免疫染色。另一方面，与IMI共同给予OMO或OME的大鼠在所有研究的毒理学参数上均有显著改善。总之，[植物名称]提取物与IMI联合处理可通过其强大的抗氧化、抗炎和抗凋亡作用预防IMI神经毒性。因此，我们建议每日摄入[植物名称]以预防杀虫剂的氧化应激介导的神经炎症应激和细胞凋亡。芳樟醇、迷迭香酸、γ-萜品烯和萜品-4-醇的分子对接研究证明了暴露于IMI后诱导的升高的iNOS和TNF-α水平恢复正常的现象。
