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首页> 外文期刊>Molecular Neurobiology >Protective Effects of Spatholobi Caulis Extract on Neuronal Damage and Focal Ischemic Stroke/Reperfusion Injury
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Protective Effects of Spatholobi Caulis Extract on Neuronal Damage and Focal Ischemic Stroke/Reperfusion Injury

机译:Spatholobi Caulis提取物对神经元损伤和局灶性缺血性卒中/再灌注损伤的保护作用

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Neuronal apoptotic cell death plays an important role in many neurological disorders, including Alzheimer's disease, Parkinson's disease, and ischemic stroke. Spatholobi Caulis (SC) has been widely used in traditional herbal medicine for the treatment of cancer, inflammation, viral infection, and anemia. However, the protective effects of SC extract (SCE) against apoptotic cell death in the brain have not been reported. We investigated the protective effects of SCE against neuronal injury etoposide-induced neurotoxicity and in rats subjected to focal transient ischemic stroke middle cerebral artery occlusion (MCAO) for 45 min, followed by 7 days of reperfusion. The in vitro study demonstrated that SCE protected cells against etoposide-induced cell viability loss in SH-SY5Y cells. Apoptotic phenotypes, such as cleaved PARP and caspase-3, and oxidative stress in etoposide-treated cells were ameliorated by SCE treatment. In MCAO-reperfusion injury, SCE promoted neuronal survival and level of brain-derived neurotrophic factor (BDNF) by reducing glial activation, oxidative stress, and apoptosis in the ipsilateral cortex. These results indicated that SCE exerted protective effects under etoposide treatment and in a MCAO-reperfusion model by reducing JNK and p38 MAPK activation. This study presents the first evidence that SCE has therapeutic potential for the treatment of ischemic stroke or neurological disorder-related cell death.
机译:神经元凋亡细胞死亡在许多神经系统疾病中起重要作用,包括阿尔茨海默病,帕金森病和缺血性卒中。 Spatholobi caulis(sc)已广泛用于传统草药治疗癌症,炎症,病毒感染和贫血。然而,尚未报告SC提取物(SCE)对大脑中凋亡细胞死亡的保护作用。我们调查了SCE对神经元损伤的保护作用依托泊苷诱导的神经毒性,并且在对局部瞬时缺血性卒中中脑动脉闭塞(MCAO)进行的大鼠45分钟,然后再灌注7天。体外研究证明,SCE保护细胞免受SH-SY5Y细胞中依托皂苷诱导的细胞活力损失的影响。通过SCE治疗改善了凋亡表型,例如切割的PARP和Caspase-3,以及依托泊苷处理的细胞中的氧化应激。在MCAO再灌注损伤中,通过降低IPsilidallal皮质中的胶质激活,氧化应激和细胞凋亡,SCE促进了神经元存活率和脑衍生的神经营养因子(BDNF)的水平。这些结果表明,通过减少JNK和P38 MAPK激活,SCE在依托吡啶处理和MCAO再灌注模型下发挥了保护作用。本研究提出了第一种证据,即SCE具有治疗缺血性卒中或神经障碍相关细胞死亡的治疗潜力。

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