Synergistic effects of auraptene and 17-β estradiol on traumatic brain injury treatment: oxidant/antioxidant status, inflammatory cytokines and pathology.

IF 1.7 4区医学 Q4 NEUROSCIENCES

International Journal of Neuroscience Pub Date : 2024-12-01 Epub Date: 2023-10-19 DOI:10.1080/00207454.2023.2269478

Zakieh Keshavarzi, Sedigheh Amiresmaili, Masoud Nazari, Elham Jafari, Mohadeseh Chahkandi, Rakesh K Sindhu

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引用次数: 0

Abstract

Objective: Despite significant advances that have been made in the treatment of traumatic brain injury (TBI), it remains a global health issue. This study aimed to investigate the synergistic effects of 17-β estradiol (E2) and auraptene (AUR) on TBI treatment.

Methods: In total, 70 adult male Wistar rats were divided randomly into ten main groups: Sham, TBI, TBI + DMSO, TBI + AUR (4 mg/kg), TBI + AUR (8 mg/kg), TBI + AUR (25 mg/kg), TBI + E2 group, TBI + AUR (4 mg/kg) + E2 group, TBI + AUR (8 mg/kg) + E2 group and TBI + AUR (25 mg/kg) + E2 group. Diffuse TBI was caused by the Marmarou process in male rats. The brain's tissues were harvested to check the parameters of oxidative stress and levels of inflammatory cytokine.

Results: The finding revealed that TBI induced a significant increase in brain edema, pro-inflammatory cytokines and oxidant levels [MDA and NO], and also a decrease in the brain's antioxidant biomarkers [GPx, SOD]. We also found that E2 and AUR (25 mg/kg) significantly preserved the levels of these biomarkers. The combination of AUR concentrations and E2 showed that this treatment efficiently preserved the levels of these biomarkers. Furthermore, the combination of E2 and AUR (25 mg/kg) c could cause the most effective synergistic interaction.

Conclusion: AUR could act synergistically with E2 to treat brain injury complications.

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Auaptene和17-β雌二醇在创伤性脑损伤治疗中的协同作用：氧化剂/抗氧化剂状态、炎性细胞因子和病理学。

目的尽管创伤性脑损伤（TBI）的治疗取得了重大进展，但它仍然是一个全球性的健康问题。本研究旨在探讨17-β雌二醇（E2）和Aurpene（AUR）对TBI治疗的协同作用。方法：70只成年雄性Wistar大鼠随机分为Sham、TBI、TBI三组 + DMSO，TBI + AUR（4 mg/kg），TBI + AUR（8 mg/kg），TBI + AUR（25 mg/kg），TBI + E2组，TBI + AUR（4 mg/kg）+E2组，TBI + AUR（8 mg/kg）+E2组和TBI + AUR（25 mg/kg）+E2组。弥漫性TBI是由雄性大鼠的Marmarou过程引起的。采集大脑组织以检查氧化应激参数和炎症细胞因子水平。结果：研究结果表明，TBI可显著增加脑水肿、促炎细胞因子和氧化剂水平[MDA和NO]，并降低大脑的抗氧化生物标志物[GPx、SOD]。我们还发现E2和AUR（25 mg/kg）显著地保持了这些生物标志物的水平。AUR浓度和E2的组合表明，这种处理有效地保持了这些生物标志物的水平。此外，E2和AUR的组合（25 mg/kg）c可引起最有效的协同作用。结论：AUR可与E2协同治疗脑损伤并发症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Journal of Neuroscience 医学-神经科学

CiteScore

5.10

自引率

0.00%

发文量

132

审稿时长

2 months

期刊介绍： The International Journal of Neuroscience publishes original research articles, reviews, brief scientific reports, case studies, letters to the editor and book reviews concerned with problems of the nervous system and related clinical studies, epidemiology, neuropathology, medical and surgical treatment options and outcomes, neuropsychology and other topics related to the research and care of persons with neurologic disorders. The focus of the journal is clinical and transitional research. Topics covered include but are not limited to: ALS, ataxia, autism, brain tumors, child neurology, demyelinating diseases, epilepsy, genetics, headache, lysosomal storage disease, mitochondrial dysfunction, movement disorders, multiple sclerosis, myopathy, neurodegenerative diseases, neuromuscular disorders, neuropharmacology, neuropsychiatry, neuropsychology, pain, sleep disorders, stroke, and other areas related to the neurosciences.