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抗真菌提取物对黄曲霉毒素 B 诱导大鼠神经化学恶化的预防效率。

Preventive Efficiency of Ethanolic Extract Against Aflatoxin B Induced Neurochemical Deteriorations in Rats.

出版信息

Pak J Biol Sci. 2022 Jan;25(3):234-244. doi: 10.3923/pjbs.2022.234.244.

DOI:10.3923/pjbs.2022.234.244
PMID:35234014
Abstract

<b>Background and Objective:</b> Aflatoxins affect many species including humans and animals, therefore the present study was designed to investigate the protective effect of <i>Chelidonium majus</i> Ethanolic Extract (CMEE) on neurotoxicity induced by Aflatoxin B<sub>1</sub> (AFB1) in rats. <b>Materials and Methods:</b> Four groups of male Albino rats were treated orally for 28 days as follows: (1) Control group was daily given DMSO-PBS buffer (1.0 mL per rat), (2) CMEE (300 mg kg<sup>1</sup>/day) dissolved in DMSO-PBS buffer, (3) AFB1 (80 μg kg<sup>1</sup>/day) dissolved in DMSO-PBS buffer and (4) Received daily AFB1 (300 mg kg<sup>1</sup>) in combination with CMEE (300 mg kg<sup>1</sup>). <b>Results:</b> CMEE exhibits antioxidant activity <i>in vitro</i> and neuroameliorative efficiency <i>in vivo</i> as its administration in combination with AFB1 succeeded significantly in down regulating the elevated levels of inflammatory and apoptotic markers and restoring the values of neurochemical markers (AChE-ase, dopamine and serotonin) that were deteriorated by AFB1 intake. <b>Conclusion:</b> In conclusion, the neuroprotective effect of CMEE may be mediated through its antioxidant and free radical scavenging activity that proved from the data<i> </i>of ferric-reducing power ability and DPPH radical scavenging activity.

摘要

<b>背景与目的:</b>黄曲霉毒素影响包括人类和动物在内的许多物种,因此本研究旨在探讨 <i>Chelidonium majus</i> 乙醇提取物(CMEE)对黄曲霉毒素 B<sub>1</sub>(AFB1)诱导的大鼠神经毒性的保护作用。<b>材料与方法:</b>四组雄性白化大鼠经口给予以下药物治疗 28 天:(1)对照组每日给予 DMSO-PBS 缓冲液(1.0 mL/只),(2)CMEE(300 mg/kg<sup>1</sup>/天)溶于 DMSO-PBS 缓冲液中,(3)AFB1(80 μg/kg<sup>1</sup>/天)溶于 DMSO-PBS 缓冲液中,(4)每日接受 AFB1(300 mg/kg<sup>1</sup>)与 CMEE(300 mg/kg<sup>1</sup>)联合治疗。<b>结果:</b>CMEE 在体外表现出抗氧化活性,在体内具有神经改善作用,因为其与 AFB1 联合使用可显著下调升高的炎症和凋亡标志物水平,并恢复因摄入 AFB1 而恶化的神经化学标志物(乙酰胆碱酯酶、多巴胺和 5-羟色胺)的水平。<b>结论:</b>总之,CMEE 的神经保护作用可能是通过其抗氧化和自由基清除活性介导的,这从铁还原能力和 DPPH 自由基清除活性的数据中得到了证明。

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