College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Heilongjiang Veterinary Drugs and Feed Monitor, Harbin 150030, China.
Biomed Pharmacother. 2017 Jul;91:931-937. doi: 10.1016/j.biopha.2017.05.022. Epub 2017 May 13.
Alzheimer's disease (AD) is a progressive and ultimately fatal neurodegenerative diseases. Aluminum, a neurotoxic metal, is considered as the pathological hallmark and contributing factor of AD. Hypericum perforatum extract (HPE) is a neuroprotective agent that can prevent neurodegenerative pathologies through antioxidants, anti-inflammatory and regulating neurotransmitter release in animal model of neuropathy. The present study aimed to identify the potential neuroprotective of HPE on AlCl-induced AD rats. Rats were treated with AlCl for 90days to induce behavioral, biochemical, and neurochemical similar to AD. From 31thday, the rats were treated with HPE for 60days. Our results showed HPE improved cognitive function in AlCl-induced AD rats, and attenuated AlCl-induced increase in acetylcholinesterase activity and glutamic acid level as well as decreased in noradrenaline and dopamine level. In addition, HPE reversed AlCl-induced hippocampal pathology including amyloid-beta (Aβ) accumulation (elevated Aβ42 level and amyloid plaques), oxidative stress (increased reactive oxygen species level and thiobarbituric acid reactive substances level, decreased glutathione level and superoxide dismutase activity) and neuroinflammatory (increased mRNA expressions of Interleukin-1β, Interleukin-6, Tumor necrosis factor-α and major histocompatibility complex class II) in hippocampus of rats. Thus, HPE is conferred neuroprotection against AlCl-induced AD like pathology.
阿尔茨海默病(AD)是一种进行性的、最终致命的神经退行性疾病。铝是一种神经毒性金属,被认为是 AD 的病理标志和促成因素。贯叶金丝桃提取物(HPE)是一种神经保护剂,它可以通过抗氧化剂、抗炎和调节神经递质释放来预防神经病变动物模型中的神经退行性病变。本研究旨在确定 HPE 对 AlCl 诱导的 AD 大鼠的潜在神经保护作用。大鼠用 AlCl 处理 90 天,以诱导类似于 AD 的行为、生化和神经化学改变。从第 31 天开始,大鼠用 HPE 处理 60 天。我们的结果表明,HPE 改善了 AlCl 诱导的 AD 大鼠的认知功能,并减轻了 AlCl 诱导的乙酰胆碱酯酶活性和谷氨酸水平升高,以及去甲肾上腺素和多巴胺水平降低。此外,HPE 逆转了 AlCl 诱导的海马病理学,包括淀粉样β(Aβ)积累(Aβ42 水平升高和淀粉样斑块)、氧化应激(活性氧水平和硫代巴比妥酸反应物质水平升高,谷胱甘肽水平和超氧化物歧化酶活性降低)和神经炎症(白细胞介素-1β、白细胞介素-6、肿瘤坏死因子-α和主要组织相容性复合体 II 的 mRNA 表达增加)。因此,HPE 对 AlCl 诱导的 AD 样病变具有神经保护作用。