本文選題：脾虛 + 脂質(zhì)沉積��； 參考：《遼寧中醫(yī)藥大學(xué)》2016年碩士論文

【摘要】：目的:中醫(yī)認(rèn)為,脾主運(yùn)化,脾失健運(yùn)導(dǎo)致膏脂轉(zhuǎn)輸障礙。本研究從中醫(yī)病機(jī)切入,在中醫(yī)理論指導(dǎo)下,復(fù)制脾虛高脂血癥大鼠模型,從分子水平初步探討脾虛狀態(tài)對血脂水平及肝臟脂質(zhì)沉積的影響及機(jī)制。材料與方法:60只SPF級SD雄性大鼠,體重(300±10)g,適應(yīng)環(huán)境7 d,進(jìn)入實(shí)驗(yàn)過程,實(shí)驗(yàn)用大鼠按照隨機(jī)數(shù)字表法分為空白對照組20只、高脂血癥組20只、脾虛高脂血癥組20只,空白對照組繼續(xù)常規(guī)飼養(yǎng),高脂血癥組予高脂飼料喂飼,脾虛高脂血癥組采用游泳勞倦過度加飲食不節(jié)結(jié)合高脂飼料喂飼造模,造模60 d后分別稱重取材。采用間苯三酚法測定尿D-木糖排泄率,全自動生化分析儀檢測血清TC、TG、LDL-C、HDL-C、AMY水平,采用HE染色觀察肝臟形態(tài)變化,油紅O染色觀察肝臟脂質(zhì)沉積,分別采用COD-CE-PAP法和GPO-PAP法測定肝臟TC和TG含量,采用實(shí)時(shí)熒光定量反轉(zhuǎn)錄-聚合酶鏈反應(yīng)(real-time RT-PCR)及蛋白免疫印跡(Western blot)法檢測肝臟HMGCR、HL、CYP7A1、LDL-R基因m RNA和蛋白表達(dá)。統(tǒng)計(jì)學(xué)處理:采用SPSS 17.0軟件包進(jìn)行統(tǒng)計(jì)分析,采用單因素方差(One-Way ANOVA)進(jìn)行分析,統(tǒng)計(jì)結(jié)果以平均值±標(biāo)準(zhǔn)差(x±S)表示,以P0.05為差異有統(tǒng)計(jì)學(xué)意義。結(jié)果:1.脾虛狀態(tài)對高脂血癥大鼠血脂、血清AMY水平及尿D-木糖排泄率的影響實(shí)驗(yàn)結(jié)果顯示,與空白對照組相比,高脂血癥組及脾虛高脂血癥組大鼠血清TC、LDL-C水平顯著升高(均P0.01),血清HDL-C、AMY水平顯著降低(P0.05、P0.01)。與高脂血癥組相比,脾虛高脂血癥組大鼠血清TC、LDL-C水平顯著升高(P0.05、P0.01),血清HDL-C、AMY水平及尿D-木糖排泄率顯著降低(P0.05、P0.01)。2.脾虛狀態(tài)對高脂血癥大鼠肝臟形態(tài)以及肝臟脂質(zhì)沉積的影響實(shí)驗(yàn)結(jié)果顯示,與空白對照組相比,高脂血癥組及脾虛高脂血癥組肝細(xì)胞出現(xiàn)大面積脂肪變性和脂質(zhì)沉積。3.脾虛狀態(tài)對高脂血癥大鼠肝臟脂質(zhì)含量的影響實(shí)驗(yàn)結(jié)果顯示,與空白對照組相比,高脂血癥組及脾虛高脂血癥組大鼠肝臟TG、TC含量顯著升高(P0.05、P0.01)。與高脂血癥組相比,脾虛高脂血癥組大鼠肝臟TG、TC含量顯著升高(均P0.01)。4.脾虛狀態(tài)對高脂血癥大鼠肝臟HMGCR、HL、CYP7A1、LDL-R基因m RNA表達(dá)的影響實(shí)驗(yàn)結(jié)果顯示,與空白對照組相比,高脂血癥組和脾虛高脂血癥組大鼠肝臟HMGCR、HL、CYP7A1及LDL-R基因m RNA表達(dá)水平顯著降低(P0.05、P0.01)。與高脂血癥組相比,脾虛高脂血癥組大鼠肝臟HL、CYP7A1及LDL-R基因m RNA表達(dá)水平顯著降低(P0.05、P0.01),而HMGCR基因m RNA表達(dá)水平無顯著變化。5.脾虛狀態(tài)對高脂血癥大鼠肝臟HMGCR、HL、CYP7A1、LDL-R基因蛋白表達(dá)的影響實(shí)驗(yàn)結(jié)果顯示,與空白對照組相比,高脂血癥組和脾虛高脂血癥組大鼠肝臟HMGCR、HL、CYP7A1及LDL-R基因蛋白表達(dá)水平顯著降低(P0.05,P0.01)。與高脂血癥組相比,脾虛高脂血癥組大鼠肝臟HL、CYP7A1及LDL-R基因蛋白表達(dá)水平顯著降低(P0.05,P0.01),而HMGCR基因蛋白表達(dá)水平無顯著變化。結(jié)論:1.通過游泳勞倦過度加飲食不節(jié)結(jié)合高脂飼料的方法成功構(gòu)建脾虛高脂血癥大鼠模型。2.脾虛狀態(tài)加重高脂血癥大鼠血脂紊亂以及肝臟脂質(zhì)沉積。3.脾虛狀態(tài)影響肝臟膽固醇攝取及轉(zhuǎn)化相關(guān)基因m RNA及蛋白表達(dá)。
[Abstract]:Objective: Traditional Chinese medicine (TCM) thinks that the spleen is main transport and the spleen is lost and transported to the barrier of ointment and fat transfer. In this study, the rat model of spleen asthenia hyperlipidemia was replicated under the theory of traditional Chinese medicine, and the effect and mechanism of spleen deficiency on blood lipid level and liver lipid deposition were preliminarily discussed from the molecular level. Materials and methods: 60 SD male rats of SPF grade, The body weight (300 + 10) g, adapted to the environment 7 d, entered the experimental process. The experimental rats were divided into 20 rats in the blank control group according to the random number table method, 20 in the hyperlipidemia group and 20 in the spleen asthenia hyperlipidemia group. The blank control group continued to be kept regularly, the hyperlipidemia group was fed with high fat diet, and the hyperlipidemia group of the spleen deficiency hyperlipidemia group was overfed with excessive diet and diet. A model was fed with high fat feed and the model was weighed after 60 d. The urine D- xylose excretion rate was measured by the method of phenolol and three phenol. The serum TC, TG, LDL-C, HDL-C, AMY level were detected by the automatic biochemical analyzer. The liver morphologic changes were observed by HE staining, the liver lipid deposition was observed by oil red O staining, and the liver was detected by COD-CE-PAP method and GPO-PAP method respectively. The contents of TC and TG were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction (real-time RT-PCR) and protein immunoblotting (Western blot) method for detecting the m RNA and protein expression of the liver HMGCR, HL, CYP7A1, LDL-R genes. Statistical analysis was carried out by the statistical analysis of 17 software packages and the statistical analysis was carried out by single factor variance. Results the results were statistically significant with the mean value of standard deviation (x + S) and P0.05 as difference. Results: the effects of 1. spleen deficiency on blood lipid, serum AMY level and urine D- xylose excretion rate in hyperlipidemia rats showed that the serum TC and LDL-C levels in the hyperlipidemia group and the spleen asthenia hyperlipidemia group were significantly higher than those in the blank control group (all (all). P0.01), the level of serum HDL-C and AMY decreased significantly (P0.05, P0.01). Compared with the hyperlipidemia group, the serum TC, LDL-C level in the spleen asthenia hyperlipidemia group increased significantly (P0.05, P0.01), the serum HDL-C, AMY level and the excretion rate of urinary D- xylose decreased significantly. The experimental results showed that compared with the blank control group, the effects of large area fatty degeneration and lipid deposition of.3. spleen deficiency on liver lipid content in hyperlipidemia rats showed that the liver TG, T in hyperlipidemia and spleen hyperlipidemia rats were compared with those in the blank control group. C content increased significantly (P0.05, P0.01). Compared with the hyperlipidemia group, the liver TG, TC content in the spleen asthenia hyperlipidemia group increased significantly (P0.01).4. spleen deficiency state on the liver HMGCR, HL, CYP7A1, LDL-R genes in hyperlipidemia rats. The results showed that the hyperlipidemia group and the spleen deficiency hyperlipidemia group were larger than the blank control group. The expression level of M RNA in rat liver HMGCR, HL, CYP7A1 and LDL-R decreased significantly (P0.05, P0.01). Compared with hyperlipidemia group, the liver HL, CYP7A1 and LDL-R genes in the spleen asthenia hyperlipidemia rats were significantly lower than those in the hyperlipidemia group. The effects of HL, CYP7A1 and LDL-R gene protein expression showed that the expression level of HMGCR, HL, CYP7A1 and LDL-R genes in the liver of hyperlipidemia and spleen deficiency hyperlipidemia rats was significantly lower than that in the blank control group (P0.05, P0.01). Compared with the hyperlipidemia group, the liver HL, CYP7A1 and LDL-R gene proteins in the spleen asthenia hyperlipidemia rats' liver were compared with those in the hyperlipidemia group. The expression level of the HMGCR gene protein was significantly reduced (P0.05, P0.01), but the expression level of HMGCR gene protein was not significantly changed. Conclusion: the spleen deficiency hyperlipidemia model of the rat model of spleen asthenia hyperlipidemia was successfully constructed by swimming overwork and diet combined with high fat diet. The effect of.2. on blood lipid disorder in hyperlipidemia rats and the effect of.3. spleen deficiency on liver lipid deposition in rats. Liver cholesterol uptake and transformation related genes m RNA and protein expression.
【學(xué)位授予單位】：遼寧中醫(yī)藥大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2016
【分類號】：R259

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