Formononetin protects TBI rats against neurological lesions and the underlying mechanism
Formononetin protects TBI rats against neurological lesions and the underlying mechanism
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Formononetin 保护 TBI 大鼠免受神经损伤及其潜在机制。
DOI：
10.1016/j.jns.2013.12.027
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发表时间：
2014-03-15
影响因子：
4.4
通讯作者：
Ye, Yu
中科院分区：
文献类型：
--
作者：
Li, Zhengzhao;Dong, Xianhong;Ye, Yu
创伤性脑损伤（TB！）是全世界残疾或死亡的主要原因，特别是在年轻人中。因此，需要开发副作用少的有效药物。本研究旨在探讨刺芒柄花素（FN）对大鼠创伤性脑损伤（TBI）的潜在保护作用及其机制。结果表明，FN能有效提高肺结核大鼠脑组织谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）的活性。降低脑组织中丙二醛（MDA）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的含量（P < 0.01）。同时，脑积水减轻，HE染色显示脑损伤区神经细胞损伤减轻。脑组织中内源性环氧合酶-2（考克斯-2）的mRNA水平显著下调（P < 0.01）。核因子E2相关因子2（Nrf 2）蛋白表达明显上调（P < 0.01）。综上所述，我们得出结论，芒柄花素介导了有前途的抗TBI作用对神经细胞损伤，其潜在的机制与抑制脑内炎症反应和氧化应激的神经保护。(C)2013爱思唯尔有限公司版权所有。
Traumatic brain injury (TB!) is a major cause of disability or death worldwide, especially in the young. Thus, effective medication with few side effects needs to be developed. This work aimed to explore the potential benefits of formononetin (FN) on TBI rodent model and to discuss the regarding mechanism. These findings showed that FN effectively increased the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in brain tissue of TB! rats (P < 0.01), while it reduced intracephalic malonaldehyde (MDA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) concentrations (P < 0.01). Meanwhile, the hydrocephalus in the TBI rat was alleviated, and the injured nerve cell of the lesioned brain was reduced as showed in hematoxylin-eosin (HE) staining assay. In addition, the endogenous mRNA level of cyclooxygenase-2 (COX-2) in the brain of the TBI rat was significantly down-regulated (P < 0.01). Furthermore, the protein expression of nuclear factor E2-related factor 2 (Nrf2) was effectively up-regulated (P < 0.01). Taken together, we conclude that formononetin mediates the promising anti-TBI effects against neurocyte damage, whichthe underlying mechanisms are associated with inhibiting intracephalic inflammatory response and oxidative stress for neuroprotection. (C) 2013 Elsevier B.V. All rights reserved.