香芹酚的神经保护潜力:恢复氧化平衡和减轻异丙肾上腺素诱导的大鼠脑损伤标志物。

IF 3.5 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Betül Bağcı, Şeyma Aydın, Elif Dalkılınç, Selim Çomaklı, Sefa Küçükler, Selçuk Özdemir
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引用次数: 0

摘要

本研究探讨了香芹酚(CVC)对大鼠异丙肾上腺素(ISO)诱导的氧化应激、神经炎症和线粒体功能障碍的保护作用。研究结果表明,CVC治疗并没有显著改变健康大鼠的基线氧化应激水平,但通过增加抗氧化酶活性和减少脂质过氧化作用,成功减轻了iso诱导的氧化损伤,这可以通过降低MDA水平来证明。综上所述,CVC具有恢复抗氧化能力,减轻氧化损伤的作用。在神经炎症方面,ISO治疗显著增加了促炎标志物的表达,包括TNF-α、IL-1β、c-Fos、BDNF、Nfl和GFP,表明了强烈的炎症和损伤反应。在ISO暴露后注射CVC可显著降低这些标志物的表达,表明CVC可能通过调节炎症反应和减轻神经元和神经胶质损伤来发挥神经保护作用。CVC对线粒体完整性具有显著的保护作用,在CVC处理组中,线粒体损伤标志物NSE、s100B、CALP1和CALM1的mRNA表达降低,表明CVC减轻了线粒体功能障碍。分析显示,在所有组中,Aβ40、pTau181和tTau的表达水平没有显著变化,表明在研究条件下,这些生物标志物没有受到CVC治疗的实质性影响。然而,β-淀粉样蛋白的积累在两组之间存在显著差异,这表明需要进一步研究CVC在淀粉样蛋白相关疾病中的潜在意义。这些发现证实了CVC在氧化应激、炎症和线粒体损伤相关的神经系统疾病中的神经保护作用和治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroprotective potential of carvacrol: restoration of oxidative balance and mitigation of brain injury markers in isoproterenol-induced rats.

This research investigated the protective properties of Carvacrol (CVC) against Isoproterenol (ISO)-induced oxidative stress, neuroinflammation, and mitochondrial dysfunction in rats. The findings showed that CVC treatment did not significantly modify baseline oxidative stress levels in healthy rats but successfully alleviated ISO-induced oxidative damage by augmenting antioxidant enzyme activity and diminishing lipid peroxidation, as demonstrated by a reduction in MDA levels. These findings indicate that CVC can reinstate antioxidant capability and reduce oxidative damage. Concerning neuroinflammation, ISO therapy markedly increased the expression of pro-inflammatory markers, including TNF-α, IL-1β, c-Fos, BDNF, Nfl, and GFP, signifying a robust inflammatory and damage response. The injection of CVC following ISO exposure markedly decreased the expression of these markers, suggesting that CVC may exert a neuroprotective effect by regulating the inflammatory response and mitigating neuronal and glial damage. CVC demonstrated a notable protective effect on mitochondrial integrity, evidenced by the decreased mRNA expression of mitochondrial damage markers, including NSE, s100B, CALP1, and CALM1 in the CVC-treated groups, showing that CVC mitigates mitochondrial dysfunction. The analysis revealed no significant alterations in the expression levels of Aβ40, pTau181, and tTau across all groups, indicating that these biomarkers were not substantially influenced by CVC treatment under the study's conditions. However, β-amyloid accumulation varied significantly between groups, highlighting the need for further research to explore CVC's potential implications in amyloid-related diseases. These findings endorse CVC's neuroprotective efficacy and therapeutic potential in neurological disorders associated with oxidative stress, inflammation, and mitochondrial impairment.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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