由于其特性，清酒可能会阻止帕金森病的进展，然而，还没有研究探索其影响。这项初步研究旨在使用斑马鱼模型评估清酒补充剂对帕金森病的影响。60条鱼被分为六组：对照组，鱼藤酮(ROT),并以25、50、75和100mg/L的浓度（25S，50S,75S,和100S）。治疗28天后，过氧化氢酶(CAT)的行为反应和活性，超氧化物歧化酶（SOD），还原型谷胱甘肽（GSH），和谷胱甘肽-S-转移酶（GST），以及TNF-α的表达，IL-1β,和COX-2进行评估。结果表明，鱼藤酮给药显著减少杂交数（P=0.001），顶部区域的条目(P=0.001)，和在顶部区域花费的时间（P=0.001）。与对照组相比，它还显着增加了TBARS和SH的水平（P=0.001）。鱼藤酮显著降低CAT，SOD,和GSH活动，同时提高GST水平。此外，上调TNF-α的表达(P=0.001),IL-1β（P=0.001），和COX-2(P=0.001)。补充清酒，特别是在更高的剂量下，逆转鱼藤酮对行为的不利影响，氧化，和炎症反应。总之,清酒显示出预防帕金森病的希望，等待进一步的临床研究。
Sake may potentially halt the progression of Parkinson\'s disease due to its properties, yet no studies have explored its effects. This preliminary study aimed to assess the impact of sake supplementation on Parkinson\'s disease using a zebrafish model. Sixty fish were divided into six groups: control, rotenone (ROT), and groups administered rotenone along with sake at concentrations of 25, 50, 75, and 100 mg/L (25S, 50S, 75S, and 100S). After 28 days of treatment, behavioral responses and the activities of catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione-S-transferase (GST), as well as the expressions of TNF-α, IL-1β, and COX-2, were evaluated. The results indicated that rotenone administration significantly reduced crossing number (P = 0.001), entries in the top area (P = 0.001), and time spent in the top area (P = 0.001). It also markedly increased levels of TBARS and SH compared to the control group (P = 0.001). Rotenone significantly decreased CAT, SOD, and GSH activities while increasing GST levels. Furthermore, it upregulated the expressions of TNF-α (P = 0.001), IL-1β (P = 0.001), and COX-2 (P = 0.001). Supplementation with sake, particularly at higher doses, reversed the adverse effects of rotenone on behavioral, oxidative, and inflammatory responses. In conclusion, sake shows promise for preventing Parkinson\'s disease pending further clinical studies.
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