【摘要】：本實驗?zāi)康氖翘骄烤G原酸對脂多糖誘導(dǎo)大鼠慢性肝臟損傷的保護(hù)作用。實驗首先研究了膳食添加綠原酸對正常生理狀態(tài)下大鼠血液和肝臟中內(nèi)源性代謝物的影響。隨后以長期低劑量的脂多糖應(yīng)激建立大鼠慢性肝臟損傷模型，研究綠原酸對大鼠的生長性能、血液生化指標(biāo)、肝臟指數(shù)、肝臟形態(tài)結(jié)構(gòu)、肝臟抗氧化指標(biāo)、肝臟能量代謝指標(biāo)的影響，進(jìn)一步采用核磁共振代謝組學(xué)的方法來研究綠原酸對慢性肝臟損傷大鼠血液和肝臟中內(nèi)源性代謝物的影響。探討綠原酸對大鼠慢性肝臟損傷的保護(hù)作用及其可能的機制。 結(jié)果表明：(1)綠原酸引起了正常生理狀態(tài)下大鼠血液和肝臟中內(nèi)源性代謝物的變化，與正常組相比，綠原酸顯著增加了正常生理狀態(tài)下大鼠血液中脂蛋白、甘氨酸和不飽和脂肪酸的含量(P0.05)，顯著降低了β-羥基丁酸、乳酸、乙酰乙酸、丙酮酸、琥珀酸和檸檬酸的含量(P0.05)，顯著增加了肝臟水溶性提取物谷胱甘肽的含量(P0.05)；(2)與脂多糖組相比，綠原酸顯著降低了由脂多糖引起的大鼠末體重、平均日增重和食物轉(zhuǎn)化率的升高(P＜0.05)；顯著降低了大鼠血清中ALT和AST活性以及GLU和TG含量(P＜0.05)；顯著升高肝臟組織中ALT和AST活性以及血液中TP的含量(P＜0.05)；HE染色顯示，綠原酸能夠明顯改善慢性肝臟損傷大鼠的肝組織結(jié)構(gòu)；顯著升高大鼠肝臟組織中SOD活性(P＜0.05)，顯著降低肝臟組織中MDA含量(P＜0.05)；顯著升高大鼠肝臟組織中ATP的含量(P＜0.05)；(3)通過代謝組學(xué)的方法測定大鼠血清和肝臟內(nèi)源性代謝物含量的變化，發(fā)現(xiàn)長期脂多糖應(yīng)激抑制了大鼠機體的能量代謝，氨基酸代謝和谷胱甘肽代謝途徑；綠原酸能夠通過促進(jìn)能量代謝，氨基酸代謝和谷胱甘肽代謝途徑明顯改善了脂多糖誘導(dǎo)的大鼠慢性肝臟損傷。 綜上所述，綠原酸對脂多糖應(yīng)激引起的大鼠慢性肝臟損傷具有一定的保護(hù)作用。甘氨酸和谷胱甘肽可能是綠原酸在機體內(nèi)具有生物學(xué)活性的潛在生物標(biāo)志物。綠原酸能夠通過促進(jìn)能量代謝，氨基酸代謝和谷胱甘肽代謝等途徑，，明顯改善了脂多糖誘導(dǎo)的大鼠機體脂質(zhì)代謝紊亂、肝功能損傷、肝臟氧化損傷、肝臟線粒體損傷以及能量代謝障礙。
[Abstract]:The aim of this study was to investigate the protective effect of Lv Yuan acid on lipopolysaccharide induced chronic liver injury in rats. The effects of dietary supplementation of Lv Yuan acid on endogenous metabolites in blood and liver of rats under normal physiological conditions were studied. Then the chronic liver injury model of rats was established by long-term low dose lipopolysaccharide stress to study the growth performance, blood biochemical index, liver morphology, liver antioxidant index of Lv Yuan acid in rats. The effect of Lv Yuan acid on the endogenous metabolites in blood and liver of chronic liver injury rats was studied by nuclear magnetic resonance (NMR) method. To investigate the protective effect of Lv Yuan acid on chronic liver injury in rats and its possible mechanism. The results showed that: (1) Lv Yuan acid induced the changes of endogenous metabolites in blood and liver of rats under normal physiological condition. Compared with normal group, Lv Yuan acid significantly increased lipoprotein in blood of rats under normal physiological condition. The contents of glycine and unsaturated fatty acids (P0.05) significantly decreased the contents of 尾 -hydroxybutyric acid, lactic acid, acetoacetic acid, pyruvate, succinic acid and citric acid (P0.05), and significantly increased the content of glutathione (P0.05). (2) compared with lipopolysaccharide group, Lv Yuan acid significantly decreased the end weight, average daily gain and food conversion rate of rats induced by lipopolysaccharide (P < 0. 05), decreased the activities of ALT and AST, and the contents of GLU and TG in serum of rats (P < 0. 05). The activities of ALT and AST in liver tissue and the content of TP in blood were significantly increased (P < 0. 05). The results of HE staining showed that Lv Yuan acid could significantly improve the liver structure of chronic liver injury rats. The activity of SOD in rat liver tissue was significantly increased (P < 0. 05), the content of MDA in liver tissue was decreased (P < 0. 05), the content of ATP in rat liver tissue was significantly increased (P < 0. 05). (3) the changes of endogenous metabolites in serum and liver were determined by the method of metabolomics. It was found that long-term lipopolysaccharide stress inhibited the metabolism of energy, amino acid and glutathione in rats. Lv Yuan acid can improve the chronic liver injury induced by lipopolysaccharide in rats by promoting energy metabolism amino acid metabolism and glutathione metabolism pathway. In conclusion, Lv Yuan acid has a protective effect on chronic liver injury induced by lipopolysaccharide stress in rats. Glycine and glutathione may be potential biomarkers of Lv Yuan acids in vivo. Through promoting energy metabolism, amino acid metabolism and glutathione metabolism, Lv Yuan acid can significantly improve lipid metabolism disorder, liver function injury and liver oxidative damage induced by lipopolysaccharide in rats. Liver mitochondrial damage and energy metabolism disorders.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R965

【參考文獻(xiàn)】

相關(guān)期刊論文 前9條

1 劉安軍;馬天嬌;陳影;王云霞;陶東川;張會;;蝦青素對四氯化碳致小鼠急性肝損傷的保護(hù)作用[J];現(xiàn)代食品科技;2010年11期

2 劉安軍;王雅靜;鄭捷;鄧穎;滕安國;劉彥平;張春霞;;富鉻鹽藻對小鼠酒精性肝損傷的保護(hù)作用[J];現(xiàn)代食品科技;2011年12期

3 陳紹華;王亞琴;羅立新;;天然產(chǎn)物綠原酸的研究進(jìn)展[J];食品科技;2008年02期

4 ;Modulating Effects of Chlorogenic Acid on Lipids and Glucose Metabolism and Expression of Hepatic Peroxisome Proliferator-activated Receptor-α in Golden Hamsters Fed on High Fat Diet[J];Biomedical and Environmental Sciences;2009年02期

5 樊迎;王常青;王菲;于書佳;連偉帥;原敏;;小黑豆乳清蛋白和水解多肽對小鼠急性肝損傷的保護(hù)作用[J];食品科學(xué);2013年05期

6 湯超;湯文凡;黃玉琴;李亞坤;趙超;沈雪蓮;韓強;劉朝奇;;木瓜發(fā)酵液對小鼠四氯化碳誘發(fā)肝損傷的防護(hù)作用[J];食品科學(xué);2013年13期

7 王欣;董丹丹;邢曉越;李煒;李冰;;姜黃素干預(yù)對無機砷暴露小鼠急性肝臟損傷的拮抗作用[J];中國工業(yè)醫(yī)學(xué)雜志;2012年06期

8 黃志卓;常翠青;;氯原酸調(diào)節(jié)糖脂代謝的研究進(jìn)展[J];衛(wèi)生研究;2008年05期

9 劉穎;郭明曄;白根本;;綠原酸的研究進(jìn)展[J];中藥材;2012年07期

本文編號：2170542