Neuroprotective effects of sodium molybdate in a beta-amyloid–induced rat model of Alzheimer’s disease: An In Vivo preclinical study

IF 3.6 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Trace Elements in Medicine and Biology Pub Date : 2025-10-06 DOI:10.1016/j.jtemb.2025.127774

Fatemeh Shahsavari, Akram Eidi, Fattah Sotoodehnejadnematalahi

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引用次数: 0

Abstract

Background

Molybdenum, as a trace element, exhibits various pharmacological properties, including antioxidant, anti-inflammatory, and free radical-scavenging activities. This study aimed to evaluate the effects of sodium molybdate on neurotoxicity induced by beta-amyloid (Aβ) in adult male Wistar rats.

Methods

Forty-eight rats were randomly divided into eight groups: Healthy control group, Experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily), Alzheimer's control group (intrahippocampal injection of Aβ bilaterally), and Alzheimer's experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily) for 30 consecutive days following Aβ injection. Histopathological changes in the hippocampus were assessed using Hematoxylin and Eosin staining, and amyloid plaques were evaluated via Congo Red staining. The expression levels of GFAP and S100 proteins were investigated by immunohistochemistry, and changes in the expression level of Bax/Bcl2 ratio were evaluated by Real-time PCR in the hippocampus.

Findings

Our results revealed a dose-dependent attenuation of neuronal degeneration, and reduced amyloid plaque formation in the Alzheimer's experimental groups following sodium molybdate administration. Treatment with sodium molybdate at doses of 0.2 and 0.4 mg/kg significantly reduced the levels of both S100 and GFAP proteins (P < 0.05 and P < 0.001 respectively) compared to the Alzheimer's control group. Furthermore, sodium molybdate administration at a dose of 0.1 mg/kg significantly reduced the Bax/Bcl2 expression ratio (P < 0.05), with greater reductions observed at 0.2 and 0.4 mg/kg doses (P < 0.01).

Conclusion

The results of this study suggest that sodium molybdate may exert protective effects against neurological disorders caused by Aβ in a rat model of Alzheimer’s disease.

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钼酸钠在β -淀粉样蛋白诱导的老年痴呆症大鼠模型中的神经保护作用：一项体内临床前研究

背景：钼作为一种微量元素，具有多种药理特性，包括抗氧化、抗炎和自由基清除活性。本研究旨在探讨钼酸钠对成年雄性Wistar大鼠β -淀粉样蛋白（Aβ）神经毒性的影响。方法：48只大鼠随机分为8组：健康对照组、试验组（0.1、0.2、0.4 mg/kg / d）、阿尔茨海默病对照组（双侧海马内注射Aβ）、阿尔茨海默病试验组（0.1、0.2、0.4 mg/kg / d），连续30 d。采用苏木精和伊红染色评估海马组织病理学变化，采用刚果红染色评估淀粉样斑块。免疫组化法检测GFAP和S100蛋白表达水平，Real-time PCR法检测海马组织Bax/Bcl2比值表达水平的变化。研究结果：我们的研究结果显示，在服用钼酸钠后，阿尔茨海默氏症实验组的神经元变性呈剂量依赖性衰减，淀粉样斑块形成减少。0.2和0.4 mg/kg剂量的钼酸钠治疗显著降低了S100和GFAP蛋白的水平（P ）。结论：本研究结果提示钼酸钠可能对阿尔茨海默病大鼠模型中a β引起的神经系统疾病具有保护作用。

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来源期刊

Journal of Trace Elements in Medicine and Biology 医学-内分泌学与代谢

CiteScore

6.60

自引率

2.90%

发文量

202

审稿时长

85 days

期刊介绍： The journal provides the reader with a thorough description of theoretical and applied aspects of trace elements in medicine and biology and is devoted to the advancement of scientific knowledge about trace elements and trace element species. Trace elements play essential roles in the maintenance of physiological processes. During the last decades there has been a great deal of scientific investigation about the function and binding of trace elements. The Journal of Trace Elements in Medicine and Biology focuses on the description and dissemination of scientific results concerning the role of trace elements with respect to their mode of action in health and disease and nutritional importance. Progress in the knowledge of the biological role of trace elements depends, however, on advances in trace elements chemistry. Thus the Journal of Trace Elements in Medicine and Biology will include only those papers that base their results on proven analytical methods. Also, we only publish those articles in which the quality assurance regarding the execution of experiments and achievement of results is guaranteed.