Ayşe ÇAKIR GÜNDOĞDU, Fatih Kar
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摘要

脓毒症,它的发展与触发不受控制的炎症反应,导致多器官损伤和功能障碍。在败血症中发生的神经炎症导致中枢神经系统不同程度的恶化。由硼和氮组成的六方氮化硼(h-BN)纳米颗粒具有潜在的生物医学应用价值,并且动物耐受性良好。研究表明,氢氮化硼纳米颗粒具有抗氧化特性。虽然其中存在硼的抗炎特性,但h-BN纳米颗粒对全身性炎症或神经炎症的有效性尚不清楚。因此,本研究的目的是研究氢氮化硼纳米颗粒对脂多糖(LPS)诱导的大鼠脑炎症的潜在保护作用。采用5 mg/kg腹腔注射LPS诱导大鼠脓毒症。在LPS注射前24 h分别给予50 μg/kg和100 μg/kg浓度的h- bn纳米颗粒。为了评估h-BN纳米颗粒对脓毒症诱导的神经变性的预防作用,除了测量脑组织中的促炎、氧化应激和凋亡标志物外,还对大脑皮层和海马进行了组织病理学检查。我们的ELISA结果表明,h-BN纳米颗粒通过降低lps诱导的肿瘤坏死因子-α (TNF-α)和白细胞介素-1β (IL-1β)水平的升高来抑制大脑炎症。h-BN纳米颗粒降低氧化应激指数,降低细胞色素c和caspase-3水平,这是固有凋亡途径的组成部分。我们的组织病理学分析表明,脑皮层和海马的神经元和神经胶质损伤也被h-BN纳米颗粒处理所阻止。这些结果表明,h-BN纳米颗粒可能通过其抗炎、抗氧化和抗凋亡的特性对败血症诱导的神经变性具有神经保护作用。
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Hekzagonal Boron Nitrür Nanopartikülleri Septik Sıçan Beyninde Nörodejenerasyonu Önler
Sepsis, which develops with the triggering of an uncontrolled inflammatory response, causes multiple organ damage and dysfunction. Neuroinflammation occurring in sepsis causes varying degrees of deterioration in the central nervous system. Hexagonal boron nitride (h-BN) nanoparticles composed of boron and nitrogen have potential biomedical applications and are well tolerated by animals. Research has indicated that h-BN nanoparticles exhibit antioxidative characteristics. Although the anti-inflammatory properties of the boron present in them, the effectiveness of h-BN nanoparticles on systemic inflammation or neuroinflammation is unknown. Thus, the aim of this research was to investigate the potential protective benefits of h-BN nanoparticles against inflammation induced by lipopolysaccharide (LPS) in rat brains. An intraperitoneal 5 mg/kg dose of LPS was used to induce sepsis in Sprague Dawley rats. h-BN nanoparticles were given at 50 μg/kg and 100 μg/kg concentrations 24 h before LPS injection. To assess the prophylactic effect of h-BN nanoparticles in sepsis-induced neurodegeneration, besides measuring pro-inflammatory, oxidative stress, and apoptosis markers in brain tissues, the cerebral cortex and hippocampus were also examined histopathologically. Our ELISA results show that h-BN nanoparticles inhibit inflammation in the brain as evidenced by the reduction in LPS-induced increase in tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) levels. h-BN nanoparticles diminished the oxidative stress index and lowered cytochrome c and caspase-3 levels, components of the intrinsic apoptotic pathway. Our histopathological analyzes demonstrated that neuronal and neuroglial damage in the cerebral cortex and hippocampus was also prevented by the treatment of h-BN nanoparticles. These results implicated that h-BN nanoparticles could have a neuroprotective effect against sepsis-induced neurodegeneration through their anti-inflammatory, antioxidant, and anti-apoptotic properties.
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