ASIA unversity:Item 310904400/86915
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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/86915


    Title: GABA tea ameliorates cerebral cortex apoptosis and autophagy in streptozotocin-induced diabetic rats
    Authors: 黃志揚;Huang, Chih-yang;郭薇雯;Hsueh-Fang, W;Wang, Hsueh-Fang;Li, Cheng-Jyh;Lin, Cheng-Jyh;Lin, Yueh-Min;Lin, Yueh-Min;Che, Jia-Long;Chen, Jia-Long;Kuo, Chia-Hua;Kuo, Chia-Hua;Che, Ping-Kun;Chen, Ping-Kun;Li, Jing-Ying;Lin, Jing-Ying;*
    Contributors: 生物科技學系
    Keywords: GABA tea;Diabetes mellitus;Apoptosis;Autophagy
    Date: 2014
    Issue Date: 2014-11-07 06:49:45 (UTC+0)
    Abstract: The γ-aminobutyric acid (GABA) tea is popular by consumers in Asia in recent years. This study investigated the effects of GABA tea on apoptosis and autophagy in the cerebral cortex of streptozotocin (STZ)-induced diabetic rats. Thirty-four male Wistar rats at 8 weeks of age were randomly divided into control group, STZ-induced (60 mg/kg, i.p.) diabetes (DM), and DM rats with water GABA tea extracts of containing GABA either 3.01 or 30.1 μg/rat per day for 6 weeks. Treatment with GABA tea dose-dependently lowered blood glucose level in the diabetic rats compared with vehicle. GABA tea reduced the diabetic-induced Fas-dependent and mitochondrial-dependent apoptotic pathway in the diabetic cerebral cortex compared with vehicle, the evidence for which is based on decreases in Fas, activated caspase-8, pro-apoptotic t-Bid, Bax, cytosolic cytochrome c, activated caspase-9 and activated caspase-3. GABA tea also reduced the diabetic-induced autophagy. The results suggest that GABA tea obviously inhibits diabetic-induced apoptosis in the cerebral cortex through the suppression of Fas and mitochondrial pathways. These findings provide the possible diabetes-related apoptotic and autophagy pathways in the cerebral cortex and suggest that GABA tea treatment has the potential to prevent diabetic brain abnormality.
    Relation: Journal of Functional Foods;6:534–544
    Appears in Collections:[Department of Biotechnology] Journal Article

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