本文關(guān)鍵詞：綠原酸對大鼠肝臟脂肪代謝調(diào)節(jié)機(jī)制研究　出處：《湖南農(nóng)業(yè)大學(xué)》2014年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 綠原酸 高脂飼料 肝臟 核受體 酶基因

【摘要】：目的：研究綠原酸對高脂誘導(dǎo)的肝臟脂肪代謝紊亂的分子作用機(jī)制。 背景：生活方式和生活質(zhì)量的改變,使得肥胖正在成為公共衛(wèi)生一大難題,而肝臟作為機(jī)體第一大能量代謝器官,在脂肪攝入過量的情況下,易于發(fā)生脂肪代謝紊亂,嚴(yán)重將會病變?yōu)榉蔷凭灾靖窝�。近年�?隨著肥胖患病率發(fā)生居高不下,由此引發(fā)的一系列慢性疾病成為了診療難題。由于臨床藥物的副作用和療效等問題,調(diào)整飲食結(jié)構(gòu),可以作為改善機(jī)體脂肪代謝,預(yù)防肝臟脂肪代謝紊亂的重要途徑。天然產(chǎn)物綠原酸廣泛存在于膳食中,在抗氧化,抗病毒,降血脂等多種功效方面表現(xiàn)優(yōu)良。但是,綠原酸對肝臟脂肪代謝的調(diào)節(jié)機(jī)制有待深入研究。 方法：體重130±10g的雄性SD大鼠,經(jīng)過8天適應(yīng)期喂養(yǎng)后,隨機(jī)分成五組：空白對照組(NC組),每天灌胃超純水；高脂肪模型組(HFD組),每天灌胃超純水；低劑量綠原酸組(HFD-LC組),按照20mg·kg-1·d-1劑量灌胃綠原酸；高劑量綠原酸組(HFD-HC組),按照90mg·kg-1·d-1劑量灌胃綠原酸；陽性對照組(HFD-ROS組),按照羅格列酮3mg·kg-1·d-1劑量進(jìn)行灌胃；其中空白對照組投放普通飼料,其余各組每天投放高脂肪飼料。12周后,大鼠麻醉處死后,眼球采血,檢測血清TC, TG, LDL-c, HDL-c, FFA, ALT,瘦素。檢測肝臟組織TG, Real time PCR檢測LXRα、 SREBP-1c、ACCα、FAS、AP2、FAT/CD36、LPL、HMGCR、PPARa、CPT-1和CPT-2mRNA的表達(dá)。HE染色法方法觀察肝臟組織病理變化。 結(jié)果：綠原酸可以對高脂飼料誘導(dǎo)的體重增加起到抑制作用,并且改善血脂譜,改善高脂誘發(fā)的瘦素抵抗。綠原酸可以降低肝臟的重量、緩解肝臟脂肪的累積,基因表達(dá)結(jié)果揭示,第一,綠原酸降低了大鼠肝組織的LXRα、SREBP-1c表達(dá),mRNA進(jìn)而調(diào)控下游與脂肪合成有關(guān)表達(dá)；第二,綠原酸上調(diào)了大鼠肝ACCα、FAS mRNA組織表達(dá),進(jìn)而激活了和脂肪酸氧化相關(guān)的基因PPARa mRNA表達(dá),CPT-1、CPT-2促進(jìn)脂肪分解代謝；第三,綠原酸可以降低與脂肪酸攝入相關(guān)的基因的AP2、FAT/CD36表達(dá)。HE染色組織切片結(jié)果顯示,高脂飼料引起肝臟組織出現(xiàn)大量空泡,mRAN脂滴積累明顯,綠原酸可以有效明顯減少脂肪引起的空泡,抑制肝臟組織中脂肪累積。結(jié)論：綠原酸可以通過調(diào)節(jié)肝臟核受體及其下游基因表達(dá),有效改善高脂飼料喂 飼誘發(fā)的大鼠肝臟脂肪代謝紊亂,抑制脂肪在肝臟組織的積累。
[Abstract]:Aim: to study the molecular mechanism of chlorogenic acid on fatty metabolic disorder induced by hyperlipidemia. Background: changes in lifestyle and quality of life have made obesity a public health challenge, while the liver, as the body's number one energy metabolism organ, is suffering from excessive fat intake. It is easy to develop the disorder of fat metabolism, which will change into non-alcoholic fatty liver disease. In recent years, the prevalence rate of obesity remains high. A series of chronic diseases caused by this has become a difficult problem in diagnosis and treatment. Because of the side effects and effects of clinical drugs, the adjustment of dietary structure can be used to improve the body fat metabolism. An important way to prevent hepatic fat metabolism disorder. Chlorogenic acid, a natural product, is widely found in diet, and has good performance in antioxidant, antiviral, and lipid-lowering functions. The regulation mechanism of Lv Yuan acid on hepatic fat metabolism needs further study. Methods: male SD rats weighing 130 鹵10 g were randomly divided into five groups after feeding for 8 days. Hyperlipidemia model group, HFD group, daily intragastric infusion of ultra-pure water; The low dose Lv Yuan acid group (HFD-LC group) was administrated intragastrically according to 20mg 路kg-1 路d-1 dose. The high dose Lv Yuan acid group was treated by gastric instillation of Lv Yuan acid according to 90 mg 路kg-1 路d-1 dose of HFD-HC group. The positive control group (HFD-ROS group) was given rosiglitazone (3mg 路kg-1 路d-1) by gavage. The blank control group was fed with normal diet, the other groups were given high fat diet for 12 weeks. After the rats were killed under anesthesia, blood was collected from their eyeballs and serum TC-, TG-, LDL-c were detected. HDL-c, FFA, alt, leptin. Liver TGs, Real time PCR, LXR 偽 and SREBP-1ACC 偽 were detected. The expression of CPT-1 and CPT-2mRNA in AP2FAT-CD36 LPLX HMGCRT and PPARaN. The pathological changes of liver tissue were observed by HE staining. Results: Lv Yuan acid could inhibit the weight gain induced by high fat diet, improve the blood lipid profile and improve leptin resistance induced by high fat diet. Lv Yuan acid could reduce the weight of liver. The results of gene expression showed that: first, chlorogenic acid decreased the expression of LXR 偽 -SREBP-1c in rat liver and regulated the expression of LXR 偽 SREBP-1c downstream. Secondly, Lv Yuan up-regulated the expression of ACC 偽 -FAS mRNA in rat liver and activated the expression of PPARa mRNA, a gene related to fatty acid oxidation. CPT-2 promotes adipose catabolism; Third, chlorogenic acid can reduce the expression of AP2FAT-CD36 in fatty acid related genes. The results of HE staining showed that high fat diet caused a large number of vacuoles in liver tissue. The accumulation of mRAN lipid droplets was obvious, and Lv Yuan could effectively reduce the fat induced vacuoles and inhibit the fat accumulation in liver tissue. Conclusion: Lv Yuan acid can regulate the expression of liver nuclear receptor and its downstream genes. Effective improvement of High Fat Feed feeding The hepatic fat metabolism disorder induced by feeding inhibited the accumulation of fat in the liver tissue.
【學(xué)位授予單位】：湖南農(nóng)業(yè)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R285.5

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