Department of Biochemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt.
Department of Histology and Cell Biology, Faculty of Human Medicine, Zagazig University, Zagazig, Egypt.
J Food Biochem. 2021 May;45(5):e13715. doi: 10.1111/jfbc.13715. Epub 2021 Mar 29.
Increased fructose consumption is among bad nutritional habits that contribute to increased incidence of neurodegenerative diseases. We proposed that coffee, the most popular beverage worldwide, may protect against the progression of Alzheimer's disease (AD). We investigated the protective potential of decaffeinated green coffee bean extract (GCBE) and the possible potentiation of pioglitazone (PIO) effects by decaffeinated GCBE in fructose-induced AD in rats. Twenty-four rats [12-untreated and 12-pre-treated (for 4 weeks) with GCBE] consumed drinking water supplemented with 10% fructose for 18 weeks. Twelve of these rats (6-GCBE-untreated and 6-GCBE-pre-treated) were treated orally with PIO starting on the 13th week for 6 weeks. Prophylactic administration of GCBE attenuated oxidative damage (increased cortical reduced glutathione and superoxide dismutase activity), while decreased malondialdehyde. It retarded the activation of acetylcholine esterase, increased acetylcholine level in the cortex of fructose-induced AD. It also impeded the upregulation of beta-secretase-1and the accumulation of Aβ plaques that were induced by fructose drinking. With PIO therapy, GCBE showed better effects alleviating oxidative stress and Aβ extracellular plaques formation, while improving cholinergic activity, learning, and memory ability. In conclusions, the consumption of GCBE may protect against the development of AD and delay the progression of AD when given with PIO. PRACTICAL APPLICATIONS: Decaffeinated dietary supplement of green coffee bean extract attenuated the deleterious consequences of fructose-induced Alzheimer's disease in rats. It improved the antioxidant status and cortical cholinergic activity, while hindered the changes responsible for amyloid plaque formation. It also improved the impaired learning and memory. These results, if confirmed by clinical studies, may recommend the consumption of decaffeinated green coffee beans extract as dietary supplement or as a regular beverage to protect against AD in individuals with family history or early signs of AD. With pioglitazone, such dietary supplement improved pioglitazone efficacy and delayed the progression of AD.
摄入过多的果糖是导致神经退行性疾病发病率上升的不良饮食习惯之一。我们提出，咖啡是世界上最受欢迎的饮料，可能有助于预防阿尔茨海默病（AD）的进展。我们研究了脱咖啡因绿咖啡豆提取物（GCBE）的保护潜力，以及脱咖啡因 GCBE 对果糖诱导的 AD 大鼠中吡格列酮（PIO）作用的可能增强作用。24 只大鼠[12 只未经治疗和 12 只经 GCBE 预处理（4 周）]饮用添加 10%果糖的饮用水 18 周。其中 12 只大鼠（6 只 GCBE 未治疗和 6 只 GCBE 预处理）从第 13 周开始口服 PIO 治疗 6 周。预防性给予 GCBE 可减轻氧化损伤（增加皮质还原型谷胱甘肽和超氧化物歧化酶活性），同时降低丙二醛水平。它延缓了乙酰胆碱酯酶的激活，增加了果糖诱导的 AD 皮质中的乙酰胆碱水平。它还阻止了由果糖摄入引起的β-分泌酶-1的上调和 Aβ 斑块的积累。用 PIO 治疗时，GCBE 显示出更好的缓解氧化应激和 Aβ 细胞外斑块形成的作用，同时改善胆碱能活性、学习和记忆能力。总之，GCBE 的摄入可能有助于预防 AD 的发展，并在与 PIO 一起使用时延缓 AD 的进展。实际应用：脱咖啡因的绿咖啡豆提取物膳食补充剂减轻了果糖诱导的 AD 大鼠的有害后果。它改善了抗氧化状态和皮质胆碱能活性，同时阻止了负责淀粉样斑块形成的变化。它还改善了受损的学习和记忆。如果这些结果得到临床研究的证实，可能会建议摄入脱咖啡因的绿咖啡豆提取物作为膳食补充剂或常规饮料，以保护有家族史或早期 AD 迹象的个体免受 AD 的侵害。与吡格列酮合用，这种膳食补充剂提高了吡格列酮的疗效，延缓了 AD 的进展。
