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The Role of 7,8-Dihydroxyflavone in Preventing Dendrite Degeneration in Cortex After Moderate Traumatic Brain Injury

机译:7,8-二羟基黄酮在预防中度颅脑外伤后皮层树突变性中的作用

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Our previous research showed that traumatic brain injury (TBI) induced by controlled cortical impact (CCI) not only causes massive cell death, but also results in extensive dendrite degeneration in those spared neurons in the cortex. Cell death and dendrite degeneration in the cortex may contribute to persistent cognitive, sensory, and motor dysfunction. There is still no approach available to prevent cells from death and dendrites from degeneration following TBI. When we treated the animals with a small molecule, 7,8-dihydroxyflavone (DHF) that mimics the function of brain-derived neurotrophic factor (BDNF) through provoking TrkB activation reduced dendrite swellings in the cortex. DHF treatment also prevented dendritic spine loss after TBI. Functional analysis showed that DHF improved rotarod performance on the third day after surgery. These results suggest that although DHF treatment did not significantly reduced neuron death, it prevented dendrites from degenerating and protected dendritic spines against TBI insult. Consequently, DHF can partially improve the behavior outcomes after TBI.
机译:我们以前的研究表明,由可控皮质撞击(CCI)诱发的颅脑外伤(TBI)不仅会导致大量细胞死亡,而且还会使皮质中剩余的神经元发生广泛的枝晶变性。皮质中的细胞死亡和枝晶变性可能会导致持续的认知,感觉和运动功能障碍。在TBI之后,仍然没有防止细胞死亡和树突变性的方法。当我们用小分子处理动物时,通过激发TrkB激活来模仿脑源性神经营养因子(BDNF)的功能的7,8-二羟基黄酮(DHF)减少了皮质中的树突肿胀。 DHF治疗还可以防止TBI后树突状脊柱丢失。功能分析表明,DHF在术后第三天改善了旋转脚架性能。这些结果表明,尽管DHF治疗并未显着降低神经元死亡,但可以防止树突变质并保护树突棘免受TBI损伤。因此,DHF可以部分改善TBI后的行为结果。

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