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標題: | 探討繫帶水解物在D-半乳糖誘導老化小鼠模式下對認知行為障礙及腦中氧化傷害之保護功效 The protective effects of crude chalaza hydrolysates on cognitive dysfunction and oxidative damage in the brain of D-galactose induced aging mice |
作者: | Chia-Jung Chan 詹家榮 |
指導教授: | 陳億乘(Yi-Chen Chen) |
關鍵字: | D-半乳糖,繫帶水解物,認知行為障礙,抗氧化能力,抗發炎作用,海馬迴組織觀察, D-galactose,crude chalaza hydrolysates,cognitive dysfunction,antioxidant capacity,anti-inflammatory response,hippocampus histology, |
出版年 : | 2017 |
學位: | 碩士 |
摘要: | 失智症好發於老年人口,隨著全球老年人口急遽地增加,失智症已對社會造成嚴重負擔。腦中氧化上升容易造成腦部發炎反應及神經損傷進而導致認知行為障礙進而造成失智症。本實驗室先前研究發現,利用液蛋產業產生之副產物─繫帶,其經protease A水解之蛋白質水解物(protease A-digested crude chalazae hydrolysates, CCH-As)在餵飼酒精飼糧的小鼠下有抗氧化及抗發炎之功效。故本研究目標為探討CCH-As在D-半乳糖(D-galactose, DG)誘導小鼠腦內氧化壓力上升模式下對認知行為障礙及腦中氧化傷害之保護功效。
首先,相較於水解前之乾燥繫帶原料(lyophilized crude chalazae),CCH-As含有更高量的具抗氧化游離胺基酸(如Leu、Arg、Lys)及機能性雙胜肽(anserine)。由動物實驗結果顯示:在水迷宮試驗中,於DG誘導下補充CCH-As之組別能縮短(p<0.05)參考記憶試驗中搜尋平台時間,並能延長(p<0.05)空間性探測試驗中在目標象限之停留時間。由海馬迴組織切片分析可看出補充CCH-As之組別能減緩齒狀迴神經細胞皺縮的現象。雖然補充CCH-As後未能明顯地減少齒狀迴類澱粉蛋白(amyloid β-peptide, Aβ)斑塊的堆積,卻有減少腦中Aβ蛋白表現量的效果。此外,血清及腦中的抗氧化能力在CCH-As的補充下均顯著地提升(p<0.05)。而經由CCH-As的補充,腦中糖化終產物(advanced glycation end products, AGEs)蛋白表現量顯著地下降(p<0.05),且腦中AGEs受器(RAGE)基因及發炎相關基因表現(Nfκb, IL-6, and Tnfα)均有調降作用(p<0.05)。綜觀上述研究結果,CCH-As對DG誘導下產生的腦部氧化傷害及認知行為障礙有改善的效果。 As global aging populations increase rapidly, dementia, of which the best-known factor is aging, has caused heavy social burdens. The reason for causing dementia has been reported that serious oxidative damages in brains, cause inflammatory responses and neurodegenerations, thus leading to cognitive dysfunction. According to our previous study, protease A-digested crude chalazae hydrolysates (CCH-As), a byproduct in the liquid egg industry, possess antioxidant and anti-inflammatory activities in mice fed an alcohol liquid diet. The purpose of this study was to investigate the protective effects of CCH-As on cognitive dysfunction and oxidative damage in the brain of D-galactose (DG) treated mice. First, the amounts of antioxidant free amino acids (i.e. leucine, arginine, and lysine) and dipeptides (anserine) in CCH-As were higher than those of lyophilized crude chalazae, a byproduct produced from the liquid egg industry. In the in vivo study, the administration of CCH-As reduced (p<0.05) the prolonged escape latency in the reference memory test and extended (p<0.05) the searching time around the target quadrant in the probe test of DG treated mice in the Morris water maze test. In the observations of hippocampus histology, the CCH-A co-treatment attenuated the neuronal degenerations and nucleus shrinkages in the dentate gyrus area. No clear effects of the depositions of amyloid β-peptide (Aβ) in dentate gyrus area were observed, but reduced Aβ protein levels in the whole brain tissues were analyzed by the CCH-A co-treatment. In addition, the CCH-A co-treatment enhanced (p<0.05) the antioxidant capacity in both sera and brains. Moreover, the accumulation of advanced glycation end products (AGEs) in the brain tissues dramatically decreased (p<0.05) by the CCH-A co-treatment. Furthermore, AGE receptor (RAGE) gene and inflammation related gene (Nfκb, IL-6, and Tnfα) expressions were downregulated (p<0.05) as well. These results suggested that CCH-As show protective effects on brain oxidative damage and the development of cognitive dysfunction induced by DG injection. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78010 |
DOI: | 10.6342/NTU201700417 |
全文授權: | 有償授權 |
電子全文公開日期: | 2027-12-31 |
顯示於系所單位: | 動物科學技術學系 |
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