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Protective Effects of Cornel Iridoid Glycoside in Rats After Traumatic Brain Injury

机译:基角叶苷糖苷在创伤性脑损伤后大鼠大鼠的保护作用

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Cornel iridoid glycoside (CIG) is the active ingredient extracted from Cornus officinalis. Our previous studies showed that CIG had protective effects on several brain injury models. In the present study, we aimed to examine the effects and elucidate the mechanisms of CIG against traumatic brain injury (TBI). TBI was induced in the right cerebral cortex of male adult rats. The neurological and cognitive functions were evaluated by modified neurological severity score (mNSS) and object recognition test (ORT), respectively. The level of serum S100 beta was measured by an ELISA method. Nissl staining was used to estimate the neuron survival in the brain. The expression of proteins was determined by western blot and/or immunohistochemical staining. We found that intragastric administration of CIG in TBI rats ameliorated the neurological defects and cognitive impairment, and alleviated the neuronal loss in the injured brain. In the acute stage of TBI (24-72 h), CIG decreased the level of S100 beta in the serum and brain, increased the ratio of Bcl-2/Bax and decreased the expression of caspase-3 in the injured cortex. Moreover, the treatment with CIG for 30 days increased the levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), enhanced the expression of synapsin I, synaptophysin and postsynaptic density protein 95 (PSD-95), and inhibited the apoptosis-regulating factors in the chronic stage of TBI. The present study demonstrated that CIG had neuroprotective effects against TBI through inhibiting apoptosis in the acute stage and promoting neurorestoration in the chronic stage. The results suggest that CIG may be beneficial to TBI therapy.
机译:Cornel Iridoid糖苷(CIG)是从Cornus Officinalis提取的活性成分。我们以前的研究表明,CIG对几种脑损伤模型具有保护作用。在本研究中,我们旨在探讨效果并阐明CIG对创伤性脑损伤的机制(TBI)。 TBI被诱导在右脑皮层的男性成年大鼠。通过修饰的神经定量分别评分(MNS)和物体识别测试(ORT)评估神经系统和认知函数。通过ELISA方法测量血清S100β的水平。 NISSL染色用于估计大脑中神经元生存期。通过蛋白质印迹和/或免疫组织化学染色测定蛋白质的表达。我们发现,TBI大鼠中的CIG肠道尿道施用了神经缺陷和认知障碍,并减轻了受伤脑中的神经元损失。在TBI(24-72小时)的急性阶段,CIG在血清和脑中降低了S100β的水平,增加了Bcl-2 / Bax的比例,并降低了受伤皮质中Caspase-3的表达。此外,用CIG处理30天的处理增加了神经生长因子(NGF)和脑衍生的神经营养因子(BDNF)的水平,增强了Synapsin I,Synaptophysin和突触后密度蛋白质95(PSD-95)的表达,并抑制TBI慢性阶段的凋亡调节因子。本研究证明,CIG通过抑制急性阶段的凋亡并促进慢性阶段的神经衰退,对TBI进行了神经保护作用。结果表明,CIG可能对TBI治疗有益。

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