{"title":"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","authors":"Fatemeh Shahsavari, Akram Eidi, Fattah Sotoodehnejadnematalahi","doi":"10.1016/j.jtemb.2025.127774","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Molybdenum, as a trace element, exhibits various pharmacological properties<strong>,</strong> 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.</div></div><div><h3>Methods</h3><div>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 <em>Bax/Bcl2</em> ratio were evaluated by Real-time PCR in the hippocampus.</div></div><div><h3>Findings</h3><div>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 <em>Bax/Bcl2</em> expression ratio (P < 0.05), with greater reductions observed at 0.2 and 0.4 mg/kg doses (P < 0.01).</div></div><div><h3>Conclusion</h3><div>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.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"92 ","pages":"Article 127774"},"PeriodicalIF":3.6000,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Neuroprotective effects of sodium molybdate in a beta-amyloid–induced rat model of Alzheimer’s disease: An In Vivo preclinical study\",\"authors\":\"Fatemeh Shahsavari, Akram Eidi, Fattah Sotoodehnejadnematalahi\",\"doi\":\"10.1016/j.jtemb.2025.127774\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Molybdenum, as a trace element, exhibits various pharmacological properties<strong>,</strong> 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.</div></div><div><h3>Methods</h3><div>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 <em>Bax/Bcl2</em> ratio were evaluated by Real-time PCR in the hippocampus.</div></div><div><h3>Findings</h3><div>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 <em>Bax/Bcl2</em> expression ratio (P < 0.05), with greater reductions observed at 0.2 and 0.4 mg/kg doses (P < 0.01).</div></div><div><h3>Conclusion</h3><div>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.</div></div>\",\"PeriodicalId\":49970,\"journal\":{\"name\":\"Journal of Trace Elements in Medicine and Biology\",\"volume\":\"92 \",\"pages\":\"Article 127774\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2025-10-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Trace Elements in Medicine and Biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0946672X25001877\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Trace Elements in Medicine and Biology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0946672X25001877","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Neuroprotective effects of sodium molybdate in a beta-amyloid–induced rat model of Alzheimer’s disease: An In Vivo preclinical study
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.
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.