BACKGROUND There has been a recent upsurge of interest in complementary medicine, especially dietary supplements and foods functional in delaying the onset of age-associated neurodegenerative diseases. Mushrooms have long been used in traditional medicine for thousands of years, being now increasingly recognized as antitumor, antioxidant, antiviral, antibacterial and hepatoprotective agent also capable to stimulate host immune responses. RESULTS Here we provide evidence of neuroprotective action of Hericium Herinaceus when administered orally to rat. Expression of Lipoxin A4 (LXA4) was measured in different brain regions after oral administration of a biomass Hericium preparation, given for 3 month. LXA4 up-regulation was associated with an increased content of redox sensitive proteins involved in cellular stress response, such as Hsp72, Heme oxygenase -1 and Thioredoxin. In the brain of rats receiving Hericium, maximum induction of LXA4 was observed in cortex, and hippocampus followed by substantia Nigra, striatum and cerebellum. Increasing evidence supports the notion that oxidative stress-driven neuroinflammation is a fundamental cause in neurodegenerative diseases. As prominent intracellular redox system involved in neuroprotection, the vitagene system is emerging as a neurohormetic potential target for novel cytoprotective interventions. Vitagenes encode for cytoprotective heat shock proteins 70, heme oxygenase-1, thioredoxin and Lipoxin A4. Emerging interest is now focussing on molecules capable of activating the vitagene system as novel therapeutic target to minimize deleterious consequences associated with free radical-induced cell damage, such as in neurodegeneration. LXA4 is an emerging endogenous eicosanoid able to promote resolution of inflammation, acting as an endogenous "braking signal" in the inflammatory process. In addition, Hsp system is emerging as key pathway for modulation to prevent neuronal dysfunction, caused by protein misfolding. CONCLUSIONS Conceivably, activation of LXA4 signaling and modulation of stress responsive vitagene proteins could serve as a potential therapeutic target for AD-related inflammation and neurodegenerative damage.

中文翻译：

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猴头猴在大鼠脑中对细胞应激反应和脂蛋白A4表达的氧化还原调节：与阿尔茨海默氏病发病机制的相关性。

背景技术近来，对补充药物，特别是在延缓与年龄有关的神经退行性疾病的发作中起作用的饮食补充剂和食物的兴趣激增。蘑菇在传统医学中已经使用了数千年，现在已被越来越多地认为是抗肿瘤，抗氧化剂，抗病毒，抗菌和肝保护剂，它们也能够刺激宿主的免疫反应。结果在这里，我们提供了猴头猴口服给大鼠的神经保护作用的证据。口服给予生物量猴头菌素制剂3个月后，在不同的大脑区域测量了脂氧还蛋白A4（LXA4）的表达。LXA4的上调与细胞应激反应中涉及的氧化还原敏感蛋白（例如Hsp72，血红素加氧酶-1和硫氧还蛋白。在接受猴头孢属素的大鼠的大脑中，在皮质和海马体中观察到最大程度的LXA4诱导，其次是黑质，纹状体和小脑。越来越多的证据支持以下观点：氧化应激驱动的神经炎症是神经退行性疾病的根本原因。作为参与神经保护作用的重要细胞内氧化还原系统，维他命系统正在成为新型神经保护措施的神经激素潜在靶标。Vitagenes编码细胞保护性热休克蛋白70，血红素加氧酶-1，硫氧还蛋白和Lipoxin A4。现在，新兴的兴趣集中在能够激活维生素基因系统作为新型治疗靶标的分子上，以最大程度地减少与自由基诱导的细胞损伤有关的有害后果，例如神经变性。LXA4是一种新兴的内源性类花生酸，能够促进炎症消退，在炎症过程中充当内源性“制动信号”。另外，Hsp系统正在成为调节的关键途径，以防止由于蛋白质错误折叠而引起的神经元功能障碍。结论可以想象，LXA4信号的激活和应激反应性维生素基因蛋白的调节可作为AD相关炎症和神经退行性损伤的潜在治疗靶点。