Procyanidins protects against oxidative damage and cognitive deficits after traumatic brain injury

Procyanidins protects against oxidative damage and cognitive deficits after traumatic brain injury
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DOI:
10.3109/02699052.2014.968621
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发表时间:
2015-01-01
期刊:
影响因子:
1.9
通讯作者:
Liu, Baiyun
Liu, Baiyun
中科院分区:
医学4区
文献类型:
--
作者:
Mao, Xiang;Hao, Shuyu;Liu, Baiyun

文献摘要

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主要目标:氧化应激是创伤性脑损伤(TBI)的主要因素,它引发导致长期神经元功能障碍和重塑的事件。重要的是,抗氧化剂可以保护大脑免受氧化损伤,并调节大脑的能力,以科普突触功能障碍和认知impairment.Research设计:迄今为止,然而,没有研究调查的影响原花青素(PC)对认知功能障碍后TBI。方法和程序:本研究采用大鼠皮质撞击模型(CCI),观察原花青素对CCI大鼠脑损伤的保护作用,主要结果和结论:原花青素能降低脑组织中丙二醛(MDA)含量,提高谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活性。此外,原花青素治疗,提高了脑源性神经营养因子(BDNF),磷酸化cAMP反应元件结合蛋白(pCREB),总CREB和环AMP(cAMP)的水平,改善了TBI后Morris水迷宫中的认知能力。这些结果表明,原花青素似乎可以通过抗氧化活性和上调脑损伤后的氧化损伤和行为功能障碍。cAMP/CREB信号传导的调节。
Primary objective: Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates the events that result in protracted neuronal dysfunction and remodeling. Importantly, antioxidants can protect the brain against oxidative damage and modulate the capacity of the brain to cope with synaptic dysfunction and cognitive impairment.Research design: To date, however, no studies have investigated the effects of procyanidins (PC) on cognitive deficits after TBI. Methods and Procedures: In the present study, rats with controlled cortical impact (CCI) were used to investigate the protective effects of procyanidins.Main outcomes and results: The results showed that procyanidins reduced the level of malondialdehyde (MDA) and elevated the level of glutathione (GSH) and the activity of superoxide dismutase (SOD). In addition, treatment with procyanidins, which elevated the levels of brain-derived neurotropic factor (BDNF), phosphorylation-cAMP-response element binding protein (pCREB), total CREB, and cyclic AMP (cAMP), improved cognitive performance in the Morris water maze after TBI.Conclusions: These results suggest that procyanidins appear to counteract oxidative damage and behavioral dysfunction after TBI through antioxidant activity and the up-regulation of cAMP/CREB signaling.