Mechanism for gallic acid to alleviate vascular dementia in rats

碩士 === 國立臺灣大學 === 食品科技研究所 === 102 === The increased prevalence of the older generation raises important questions about their physical and mental health. Many older individuals express significant concern about the potential loss of cognitive function and the development of dementia. Vascular dement...

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Main Authors: Shu-Chin Wang, 王淑親
Other Authors: James Swi-Bea Wu
Format: Others
Language:zh-TW
Published: 2014
Online Access:http://ndltd.ncl.edu.tw/handle/58340918825308214846
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spelling ndltd-TW-102NTU052520282016-03-09T04:24:20Z http://ndltd.ncl.edu.tw/handle/58340918825308214846 Mechanism for gallic acid to alleviate vascular dementia in rats 沒食子酸減輕大鼠血管性失智之機制探討 Shu-Chin Wang 王淑親 碩士 國立臺灣大學 食品科技研究所 102 The increased prevalence of the older generation raises important questions about their physical and mental health. Many older individuals express significant concern about the potential loss of cognitive function and the development of dementia. Vascular dementia (VaD) related to stroke is generally recognized as the second most common cause of dementia after Alzheimer’s disease (AD). Only Gallic acid (3, 4, 5-trihydroxybenzoic acid) and its derivatives are among the major phenolic compounds in plants. The present study investigated the neuroprotective effect of gallic acid using a cerebral ischemic animal model. Wistar rats were fed with normal diet for 1 week, fed with normal diet supplemented with gallic acid in various doses between 10 and 100 mg/kg/day for 5 weeks, and then subjected to a two-vessel occlusion (2VO) operation with 90 min of blood occlusion followed by 48 h of reperfusion. The rats were sacrificed to take the cortex and hippocampus for analyzing the contents of proteins in the PI3k- Akt - CREB signaling pathway by western blotting. The results show that the expressions of cell survival signaling proteins PI3K, Akt and p-CREB/CREB in rats fed with gallic acid were increased compared with the control groups. The expression of p-CREB/CREB, which is a neuron survival signal, significantly increased with the dose of gallic acid at 100mg/kg/day in the feed (p < 0.05). BDNF is an important neuroprotective factor for the alleviation of ischemic brain injury in vivo by its antagonistic function against excitatory amino acids, inflammatory factors and apoptosis. The result showed that the expression of BDNF significantly increased with the dose of gallic acid at 100mg/kg/day in the feed (p < 0.05). These data showed that gallic acid helps neurons in cerebral ischemic rats to survive, probably via the activation of the PI3K-Akt-CREB-BDNF signaling pathway. Our finding support the potential for the use of gallic acid in health food to attenuate neuronal damage in ischemia condition . James Swi-Bea Wu 吳瑞碧 2014 學位論文 ; thesis 61 zh-TW
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language zh-TW
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description 碩士 === 國立臺灣大學 === 食品科技研究所 === 102 === The increased prevalence of the older generation raises important questions about their physical and mental health. Many older individuals express significant concern about the potential loss of cognitive function and the development of dementia. Vascular dementia (VaD) related to stroke is generally recognized as the second most common cause of dementia after Alzheimer’s disease (AD). Only Gallic acid (3, 4, 5-trihydroxybenzoic acid) and its derivatives are among the major phenolic compounds in plants. The present study investigated the neuroprotective effect of gallic acid using a cerebral ischemic animal model. Wistar rats were fed with normal diet for 1 week, fed with normal diet supplemented with gallic acid in various doses between 10 and 100 mg/kg/day for 5 weeks, and then subjected to a two-vessel occlusion (2VO) operation with 90 min of blood occlusion followed by 48 h of reperfusion. The rats were sacrificed to take the cortex and hippocampus for analyzing the contents of proteins in the PI3k- Akt - CREB signaling pathway by western blotting. The results show that the expressions of cell survival signaling proteins PI3K, Akt and p-CREB/CREB in rats fed with gallic acid were increased compared with the control groups. The expression of p-CREB/CREB, which is a neuron survival signal, significantly increased with the dose of gallic acid at 100mg/kg/day in the feed (p < 0.05). BDNF is an important neuroprotective factor for the alleviation of ischemic brain injury in vivo by its antagonistic function against excitatory amino acids, inflammatory factors and apoptosis. The result showed that the expression of BDNF significantly increased with the dose of gallic acid at 100mg/kg/day in the feed (p < 0.05). These data showed that gallic acid helps neurons in cerebral ischemic rats to survive, probably via the activation of the PI3K-Akt-CREB-BDNF signaling pathway. Our finding support the potential for the use of gallic acid in health food to attenuate neuronal damage in ischemia condition .
author2 James Swi-Bea Wu
author_facet James Swi-Bea Wu
Shu-Chin Wang
王淑親
author Shu-Chin Wang
王淑親
spellingShingle Shu-Chin Wang
王淑親
Mechanism for gallic acid to alleviate vascular dementia in rats
author_sort Shu-Chin Wang
title Mechanism for gallic acid to alleviate vascular dementia in rats
title_short Mechanism for gallic acid to alleviate vascular dementia in rats
title_full Mechanism for gallic acid to alleviate vascular dementia in rats
title_fullStr Mechanism for gallic acid to alleviate vascular dementia in rats
title_full_unstemmed Mechanism for gallic acid to alleviate vascular dementia in rats
title_sort mechanism for gallic acid to alleviate vascular dementia in rats
publishDate 2014
url http://ndltd.ncl.edu.tw/handle/58340918825308214846
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