A Selenium Nanocomposite Protects the Mouse Brain from Oxidative Injury Following Intracerebral Hemorrhage.
A Selenium Nanocomposite Protects the Mouse Brain from Oxidative Injury Following Intracerebral Hemorrhage.
复制标题
硒纳米复合材料可保护小鼠大脑免受脑出血后的氧化损伤
DOI：
10.2147/ijn.s293681
复制
发表时间：
2021
影响因子：
8
通讯作者：
Zhou D
中科院分区：
文献类型：
--
作者：
Yang Y;Deng G;Wang P;Lv G;Mao R;Sun Y;Wang B;Liu X;Bian L;Zhou D
研究背景脑出血（Intracerebral hemorrhage，ICH）是一种常见的神经系统危象，病死率高.氧化应激引起的继发性损伤在神经功能恶化中起着关键作用。以前，我们合成了一种多孔Se@SiO2纳米复合材料，并确定了它们在股骨头坏死中的治疗作用。这种纳米复合材料是否具有神经保护作用仍有待阐明。MethodsA多孔Se@SiO2纳米复合材料的合成，并使用CCK-8测定其生物安全性。TUNEL法检测氯化血红素对SH-SY 5 Y细胞的神经保护作用，DCFH-DA探针检测细胞内活性氧的变化。此外，在胶原酶诱导的ICH小鼠模型中评价纳米复合物对细胞凋亡、脑水肿和血脑屏障通透性的影响。结果表明，Se@SiO2处理可显著改善神经功能，提高谷胱甘肽过氧化物酶活性，降低丙二醛水平。与溶剂处理的小鼠相比，Se@SiO2处理的ICH小鼠的凋亡细胞比例、脑水肿和血脑屏障通透性显著降低。在体外，Se@SiO2纳米复合材料可通过抑制细胞内活性氧的积累，保护SH-SY 5 Y细胞免受氯化血红素诱导的细胞凋亡的影响。Se@SiO2可能是ICH和氧化应激相关脑损伤的临床治疗的潜在候选者。
BackgroundIntracerebral hemorrhage (ICH) is a common neurological crisis leading to high mortality and morbidity. Oxidative stress-induced secondary injury plays a critical role in neurological deterioration. Previously, we synthesized a porous Se@SiO2nanocomposite and identified their therapeutic role in osteonecrosis of the femoral head. Whether this nanocomposite is neuroprotective remains to be elucidated.MethodsA porous Se@SiO2nanocomposite was synthesized, and its biosafety was determined using a CCK-8 assay. The neuroprotective effect was evaluated by TUNEL staining, and intracellular ROS were detected with a DCFH-DA probe in SH-SY5Y cells exposed to hemin. Furthermore, the effect of the nanocomposite on cell apoptosis, brain edema and blood–brain barrier permeability were evaluated in a collagenase-induced ICH mouse model. The potential mechanism was also explored.ResultsThe results demonstrated that Se@SiO2treatment significantly improved neurological function, increased glutathione peroxidase activity and downregulated malonaldehyde levels. The proportion of apoptotic cells, brain edema and blood–brain barrier permeability were reduced significantly in ICH mice treated with Se@SiO2compared to vehicle-treated mice. In vitro, Se@SiO2protected SH-SY5Y cells from hemin-induced apoptosis by preventing intracellular reactive oxygen species accumulation.ConclusionThese results suggested that the porous Se@SiO2nanocomposite exerted neuroprotection by suppressing oxidative stress. Se@SiO2may be a potential candidate for the clinical treatment of ICH and oxidative stress-related brain injuries.