کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1219884 | 1494548 | 2015 | 13 صفحه PDF | دانلود رایگان |
• The intake of black tea extract (BTE) ameliorates memory and learning deficits of Alzheimeric rats.
• The BTE attenuates the enhanced activity of acetylcholine esterase (AChE) induced by Aluminium chloride.
• The BTE offers its neuroprotection by reducing the oxidative stress.
• The BTE down regulated the increased expressions of markers associated with Alzheimer's disease (AD).
• BTE consumption in drinking water reduced apoptosis during experimental AD.
Aluminium is reported to play an important role in the aetiology, pathogenesis and development of Alzheimer's disease (AD). Black tea (BT, Camellia sinensis, family – Theaceae) represents approximately 78% of total consumed tea in the world and possesses neuroprotective properties under conditions like hypoxia, ischaemia and Parkinson's disease. This research aimed to evaluate neuroprotective effect of black tea extract (BTE) on the cognitive deficits, activity of acetylcholinesterase (AChE), levels and activities of oxidant–antioxidant indices (thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)), expressions of β amyloid 1–42 (Aβ1–42) synthesis related (amyloid precursor protein (APP), β and γ secretases) and apoptotic markers (Bax, Bcl-2, cyto c, caspases 3, 8 and 9) in hippocampus and cortex of aluminium chloride (AlCl3) induced AD rats. Chronic AlCl3 administration (100 mg/kg body weight i.p.) in Wistar rats for 60 days significantly enhanced the AChE activity, memory impairment, oxidative damage, Aβ burden and apoptosis markers. Co-administration of BTE to AlCl3 rats for 60 days significantly ameliorated the aluminium induced pathological changes. Thus, it is suggested that the anti-Alzheimer role of BTE may be attributed mainly to the active components present in black tea.
Journal: Journal of Functional Foods - Volume 16, June 2015, Pages 423–435