Haghipanah Motahareh, Ghalami Fatemeh, Saadat Maryam, Abbasi-Maleki Saeid, Gholizadeh Salmani Reza Hossein, Budde Thomas, Moradikor Nasrollah
Department of Neuroscience Research, Institute for Intelligent Research, 0105 Tbilisi, Georgia.
Ramsar International Branch, Mazandaran University of Medical Sciences, Sari 4691710001, Iran.
NeuroSci. 2023 Jan 19;4(1):45-53. doi: 10.3390/neurosci4010006. eCollection 2023 Mar.
Dementia involves several factors, and it is required to administer an agent with several efficiencies for its treatment. Sake is known to have antioxidant and anti-inflammatory properties and improves the serum concentration of BDNF. This study aimed to evaluate the neuroprotective action of Japanese sake yeast on dementia of the Alzheimer disease type in rats by behavioral evaluation and neurobiochemical assessment. The rats were grouped as non-Alzheimer rats (control rats) and Alzheimer rats administrated with 0 (AD), 10 (10-AD), 20 (20-AD), 30 (30-AD), and 40 mg/kg (40-AD) of sake. Anxiety-like and depression-like behaviors, the concentrations of brain-derived neurotrophic factor (BDNF), malondialdehyde (MDA), and ferric reducing ability of plasma (FRAP) were evaluated. The expressions of IL-1β, TNF-α, and IL-6 were assessed. The results showed that Alzheimer disease caused anxiety-like and depression-like behaviors ( = 0.000), decreased the concentrations of BDNF ( = 0.000) and FRAP ( = 0.000), increased the concentration of MDA ( = 0.000), and increased the expressions of IL-1β ( = 0.000), TNF-α ( = 0.000), and IL-6 ( = 0.000). The results showed that oral gavage of sake in higher doses decreased anxiety-like and depression-like behaviors ( = 0.000), increased the concentrations of BDNF ( = 0.000) and FRAP ( = 0.000), and reduced the concentration of MDA ( = 0.000) and the expressions of IL-1β ( = 0.000), TNF-α ( = 0.000), and IL-6 ( = 0.000). In sum, Japanese sake yeast can have roles in treating dementia of the Alzheimer disease type, but its mechanisms must be assessed in future studies.
痴呆症涉及多种因素，治疗时需要使用具有多种功效的药物。已知清酒具有抗氧化和抗炎特性，并能提高脑源性神经营养因子（BDNF）的血清浓度。本研究旨在通过行为评估和神经生化评估，评价日本清酒酵母对大鼠阿尔茨海默病型痴呆的神经保护作用。将大鼠分为非阿尔茨海默病大鼠（对照大鼠）和给予0（AD）、10（10 - AD）、20（20 - AD）、30（30 - AD）和40 mg/kg（40 - AD）清酒的阿尔茨海默病大鼠。评估了焦虑样和抑郁样行为、脑源性神经营养因子（BDNF）、丙二醛（MDA）的浓度以及血浆铁还原能力（FRAP）。评估了白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的表达。结果表明，阿尔茨海默病导致焦虑样和抑郁样行为（P = 0.000），降低BDNF（P = 0.000）和FRAP（P = 0.000）的浓度，增加MDA（P = 0.000）的浓度，并增加IL-1β（P = 0.000）、TNF-α（P = 0.000）和IL-6（P = 0.000）的表达。结果表明，高剂量口服清酒可减少焦虑样和抑郁样行为（P = 0.000），增加BDNF（P = 0.000）和FRAP（P = 0.000）的浓度，并降低MDA（P = 0.000）的浓度以及IL-1β（P = 0.000）、TNF-α（P = 0.000）和IL-6（P = 0.000）的表达。总之，日本清酒酵母在治疗阿尔茨海默病型痴呆中可能发挥作用，但其机制有待未来研究评估。
