本文選題：動脈粥樣硬化 + 炎癥標(biāo)志物　； 參考：《山東大學(xué)》2016年博士論文

【摘要】：第一部分左卡尼汀對動脈粥樣硬化大鼠抗炎抗氧化的實驗研究目的：動脈粥樣硬化AS是心血管疾病的發(fā)生及發(fā)展最主要的原因,尋找能降低動脈粥樣硬化的調(diào)節(jié)物非常重要。本研究的目的在于評價左卡尼汀(左旋肉堿、乙酰-L-肉堿、ALCAR)的在Wistar大鼠中調(diào)節(jié)改善動脈粥樣硬化的能力及其在動脈粥樣硬化大鼠中抗炎、抗氧化的作用,同時對左卡尼汀發(fā)揮抗動脈粥樣硬化作用的機(jī)制進(jìn)行更深層次的研究。方法：32只Wistar大鼠隨機(jī)分為正常飲食組(對照組)、正常飲食+ALCAR組(ALCAR組)、動脈粥樣硬化組(AS組)、動脈粥樣硬化+ALCAR組(AS+ALCAR組),動脈粥樣硬化模型采用高脂飼料喂養(yǎng)+肌肉注射維生素D3+主動脈球囊損傷建立。ALCAR組及AS+ALCAR組在常規(guī)飲食或高脂飲食的基礎(chǔ)上給予進(jìn)行左卡尼汀200mg/kg/d口服。16周后,大鼠麻醉處死,取血液樣本,主動脈和心臟組織。檢測血清脂質(zhì)分布、氧化應(yīng)激物質(zhì)水平、炎癥物質(zhì)水平和脂聯(lián)素水平；HE染色觀察主動脈組織結(jié)構(gòu)；檢測主動脈組織和心臟組織氧化應(yīng)激物質(zhì)水平,檢測主動脈組織血管緊張素Ⅱ含量；Real-timeQPCR法檢測主動脈組織及心臟組織CRP、IL-1β、TNF-α和iNOS的mRNA表達(dá)；Western blot法檢測主動脈組織及心臟組織CRP、IL-1β、TNF-α和iNOS蛋白表達(dá)。數(shù)據(jù)統(tǒng)計使用SPSS 17.0軟件包進(jìn)行,多組樣本數(shù)據(jù)間比較,采用one-way ANOVA分析,多組間兩兩組間比較,如果方差齊性者,采用LSD檢驗,如果方差不齊者,采用Dunnett's T3檢驗,如果為非正態(tài)分布者,采用Mann-Whitney檢驗,P0.05表示具有顯著性統(tǒng)計學(xué)差異。結(jié)果：1.大鼠血清血脂分布情況：與對照組相比,AS組大鼠血清TC、TG、LDL-C和VLDL-C含量顯著上升,HDL-C含量顯著下降(P0.01)。與AS組相比,AS+ALCAR組大鼠血清TC、TG、LDL-C和VLDL-C含量顯著下降,HDL-C含量顯著上升(P0.01)。正常飲食給予ALCAR后,與對照組相比,大鼠血清TC、 TG、LDL-C和VLDL-C含量有一定下降趨勢,但無顯著性統(tǒng)計學(xué)差異(P0.05),HDL-C含量顯著升高(P0.05)。2.大鼠血清氧化應(yīng)激物質(zhì)水平：與對照組比較,AS組大鼠血清MDA濃度顯著升高,SOD和GSH-Px活力顯著降低(P0.01)；AS+ALCAR組大鼠與AS組大鼠相比,ALCAR可顯著降低AS大鼠血清MDA濃度,提高SOD和GSH-Px活力(P0.05,P0.01)。3.大鼠血清炎癥物質(zhì)水平：與對照組比較,AS組大鼠血清TNF-α、IL-1β和CRP含量顯著升高(P0.01)。與AS組比較,AS+ALCAR組大鼠血TNF-α、 IL-1β和CRP含量均顯著降低(P0.01)。與對照組相比,AS組大鼠血清APN濃度顯著降低(P0.05),AS+ALCAR組大鼠血清ADPN濃度較AS組無顯著性變化(P0.05)。4.大鼠主動脈組織學(xué)檢查：HE染色結(jié)果顯示,對照組、ALCAR組大鼠的血管管腔較大,管壁較薄,血管內(nèi)膜結(jié)構(gòu)完整且平滑,中膜平滑肌細(xì)胞排列規(guī)整,平行于內(nèi)彈力膜。AS組大鼠管腔較窄,管壁明顯增厚,內(nèi)皮細(xì)胞脫落,平滑肌細(xì)胞大多排列紊亂,粥樣斑塊形成,斑塊內(nèi)可見大量泡沫細(xì)胞和脂質(zhì)沉積。AS+ALCAR組較AS組明顯管腔面積大,可見斑塊的嚴(yán)重程度遠(yuǎn)遠(yuǎn)低于AS組。5.大鼠主動脈組織氧化應(yīng)激物質(zhì)水平：與對照組比較,AS組大鼠主動脈組織MDA濃度顯著升高,SOD和GSH-Px活力顯著降低(P0.01)。與AS組大鼠相比,ALCAR可顯著降低AS大鼠主動脈組織MDA濃度,提高SOD和GSH-Px活力(P0.01)。6.大鼠主動脈組織AngⅡ含量：與對照組組相比,AS大鼠主動脈AngⅡ含量顯著上升(P0.01),ALCAR組大鼠主動脈AngⅡ含量無明顯變化。與AS組相比,ALCAR可顯著降低AS大鼠主動脈AngⅡ含量(P0.05)。7.主動脈組織炎癥物質(zhì)Real-time QPCR檢測：AS可導(dǎo)致大鼠主動脈組織TNF-α、IL-1β和iNOS的mRNA相對表達(dá)量顯著增加(P0.01)。ALCAR可顯著降低由AS大鼠的主動脈組織CRP、TNF-α、IL-1β和iNOS mRNA過度表達(dá)(P0.01)。對照組和ALCAR組主動脈組織CRP、TNF-α、IL-1β和iNOS mRNA表達(dá)無明顯差異(P0.05)。8.主動脈組織炎癥物質(zhì)Western blot檢測：AS可顯著誘導(dǎo)大鼠主動脈組織CRP、TNF-α、IL-1β和iNOS蛋白高表達(dá)(P0.01)。ALCAR對AS大鼠主動脈組織CRP、TNF-α、IL-1β和iNOS蛋白表達(dá)均有顯著的下調(diào)作用(P0.01)。對照組和ALCAR組主動脈組織CRP、TNF-α、IL-1β和iNOS蛋白表達(dá)無明顯差異(P0.05)。9.心臟組織氧化應(yīng)激物質(zhì)：與對照組比較,AS組大鼠心臟組織MDA濃度顯著升高,SOD和GSH-Px活力顯著降低(P0.01)；與AS組大鼠相比,ALCAR可顯著降低AS大鼠心臟組織MDA濃度,提高SOD和GSH-Px活力(P0.05或P0.01)。10.心臟組織炎癥物質(zhì)Real-time QPCR檢測：AS可導(dǎo)致大鼠心臟組織CRP、 TNF-α、IL-1β和iNOS的nRNA相對表達(dá)量顯著增加。ALCAR可顯著降低AS大鼠的心臟組織CRP、TNF-α、IL-1β和iNOS mRNA過度表達(dá)。ALCAR組較對照組CRP、TNF-α、IL-1β和iNOS mRNA表達(dá)低,有統(tǒng)計學(xué)意義(P0.01或P0.05)。11.心臟組織炎癥物質(zhì)Western blot檢測：AS可顯著誘導(dǎo)大鼠心臟組織CRP、TNF-α、IL-1β和iNOS蛋白高表達(dá)(P0.01)。ALCAR對正常和AS大鼠心臟組織CRP、TNF-α、IL-1β和iNOS蛋白表達(dá)均有顯著的下調(diào)作用(P0.05或P0.01)。結(jié)論：1.在AS大鼠中,ALCAR可以通過調(diào)節(jié)血脂、抑制炎癥因子基因及蛋白表達(dá)、抗氧化應(yīng)激、調(diào)節(jié)動脈腎素血管緊張素系統(tǒng)來對抗動脈粥樣硬化。2. ALCAR可以降低AS大鼠心臟組織的炎癥因子的基因及蛋白的表達(dá),增加其抗氧化能力,可能與其抗冠狀動脈粥樣硬化與心肌保護(hù)有關(guān),后續(xù)需開展更深入的機(jī)制研究。第二部分左卡尼汀對冠心病不穩(wěn)定性心絞痛的臨床療效及其抗氧化抗炎的作用目的：觀察左卡尼汀對冠心病不穩(wěn)定性心絞痛患者的臨床療效及其抗氧化、抗炎的影響,進(jìn)一步探討左卡尼汀在治療冠心病中的機(jī)制。方法：以濰坊市人民醫(yī)院作為樣本來源,樣本選取時間段為2012年8月～2013年12月,選取該院心血管內(nèi)科在此時間段內(nèi)因胸痛或胸悶入院,冠狀動脈造影結(jié)果顯示至少有一支主要冠狀動脈的管腔狹窄≥50%,并符合2011年ACC/AHA制定的《2007年不穩(wěn)定性心絞痛、非段抬高心肌梗死診療指南的更新》中不穩(wěn)定性心絞痛診斷標(biāo)準(zhǔn),確診為不穩(wěn)定性心絞痛,并符合排除標(biāo)準(zhǔn)的患者115例,隨機(jī)分為兩組,對照組(n=55)給予常規(guī)冠心病藥物治療,治療組(n=60)在常規(guī)治療基礎(chǔ)上,給予左卡尼汀治療(2G/d)靜脈滴注,治療7天,改為口服每日2g到56天。觀察兩組治療前后的臨床癥狀的改善情況、血脂分布情況、一般的血生化指標(biāo)、監(jiān)測藥物的副反應(yīng),并于治療前后測定GSH-Px、MDA、hs-CRP、IL-6、 TNF-a水平。以此來評價左卡尼汀的對冠心病不穩(wěn)定性心絞痛的臨床療效及其對冠心病患者抗炎、抗氧化的作用。本研究采用統(tǒng)計軟件SPSS 17.0對數(shù)據(jù)進(jìn)行分析,如為計量資料,采用均數(shù)±標(biāo)準(zhǔn)差(x±s)的形式來表示,對照組、治療組組內(nèi)治療前后對比應(yīng)用配對t檢驗進(jìn)行數(shù)據(jù)分析,治療后對照組與治療組比較使用獨(dú)立樣本t檢驗進(jìn)行數(shù)據(jù)分析,如為計數(shù)資料,進(jìn)行x2檢驗。P0.05表示具有顯著性統(tǒng)計學(xué)差異。結(jié)果：1.隨訪情況,臨床療效比較：對照組有2例,治療組有3例患者因失去隨訪,退出試驗,隨訪過程中沒有藥物副反應(yīng)的發(fā)生。治療后治療組的總有效率為91.22%和對照組84.91%無統(tǒng)計學(xué)意義(x 2=0.53,P=0.41),但顯效率治療組47.37%明顯高于對照組24.53%(x 2=5.23,P=0.02),差異有統(tǒng)計學(xué)意義(P0.05)。2.兩組血脂情況的比較：兩組治療前TC, TG, LDL-C, HDL-C水平無差異(P0.05),治療后對照組TG, LDL-C水平較治療前明顯降低(P0.01),HDL-C水平無明顯改變(P0.05),與治療前相比治療組的TG和LDL-C水平有明顯的下降趨勢(P0.01),而HDL-C水平有上升趨勢(P0.05),治療后治療組TG水平較對照組降低更明顯(1.65±0.21 mmol/L vs 1.79±0.10 mmol/L P0.01),HDL-C水平較對照組明顯升高(1.02±0.26 mmol／L vs 0.89±0.41 mmol/L P=0.01)。TC,LDL-C和對照組無明顯差異(4.65±1.31mmol/L vs 5.05 ±1.10mmol/L P=0.08;2.55±1.06mmol/L vs 2.85±0.90 mmol/L P=0.11)。3.兩組抗氧化能力的比較：兩組治療前GSH-Px.MDA無差異(P0.05),兩組治療前后GSH-Px,MDA的比較,兩組治療前后,治療后較治療前GSH-Px均明顯升高,MDA明顯下降(P0.01),經(jīng)過治療后治療組較對照組GSH-Px升高,MDA下降更明顯(149.80±28.40 U/mL vs 125.45±23.32 U/mL P0.01; 5.99±0.52 mmol/L vs 6.25±0.60 mmol/L P=0.02)。4.兩組炎癥因子的比較：兩組治療前hs-CRP、IL-6.TNF-α無明顯差異(P0.05),兩組治療前后hs-CRP,IL-6,TNF-α明顯下降(P0.01),治療組較對照組治療后下降更為明顯(1.65±0.62mmol/L vs 2.25±0.70mmol/L P0.01; 90.93±18.13 ng/L vs 115.82±17.50 ng/L P0.01；11.85±2.85 pmol/L vs 13.25± 3.17 pmol/L P=0.02),有統(tǒng)計學(xué)意義。結(jié)論：左卡尼汀在改善冠心病不穩(wěn)定性心絞痛癥狀方面有確切療效,在常規(guī)藥物治療的基礎(chǔ)上,進(jìn)一步可以緩解臨床癥狀,并能改善血脂分布,提高抗氧化酶的活性,提高抗氧化的能力,降低脂質(zhì)過氧化反應(yīng),降低炎癥反應(yīng),治療動脈粥樣硬化,從而治療冠心病。
[Abstract]:The aim of this study is to evaluate levocarnitine (L-carnitine, acetyl -L- carnitine, ALCA, ALCA), and the aim of the experimental study of anti inflammatory and antioxidant activities of Levocarnitine in atherosclerotic rats. R) to regulate the ability to improve atherosclerosis in Wistar rats and its anti-inflammatory and anti oxidative effect in atherosclerotic rats. At the same time, the mechanism of anti atherosclerotic effect of levocarnitine was further studied. Methods: 32 Wistar rats were randomly divided into normal diet group (control group) and normal diet +ALCAR Group (group ALCAR), atherosclerotic group (group AS), atherosclerotic +ALCAR group (group AS+ALCAR), atherosclerotic models were fed with high fat feed and intramuscular injection of vitamin D3+ aortic balloon injury to establish.ALCAR group and AS+ALCAR group on the basis of conventional diet or high fat diet on the basis of levocarnitine 200mg/kg/d oral.16 weeks after oral administration. Rats were killed, blood samples, aorta and cardiac tissue were taken. Serum lipid distribution, oxidative stress level, inflammatory substance level and adiponectin level were detected; HE staining was used to observe the structure of aorta; the levels of oxidative stress in aortic and cardiac tissues were detected, and the content of angiotensin II in aorta tissue was detected; Rea The l-timeQPCR method was used to detect the expression of CRP, IL-1 beta, TNF- alpha and iNOS in the aortic tissue and cardiac tissue, and the Western blot method was used to detect the expression of CRP, IL-1 beta, TNF- alpha and iNOS protein in the aorta and heart tissues. The data statistics were carried out by the 17 software package. The ratio of multiple groups of sample data was compared with that of the 22 groups. If the homogeneity of variance, if the LSD test, if the variance is not homogeneous, Dunnett's T3 test, if the non normal distribution, Mann-Whitney test, P0.05 showed significant statistical difference. Results: 1. rats serum lipid distribution: compared with the control group, the serum TC, TG, LDL-C and VLDL-C content in the AS group was significantly higher than that of the control group. The content of HDL-C decreased significantly (P0.01). Compared with group AS, the content of TC, TG, LDL-C and VLDL-C in the AS+ALCAR group decreased significantly, and the HDL-C content increased significantly (P0.01). The level of oxidative stress substance in serum of (P0.05).2. rats was significantly increased: compared with the control group, the concentration of MDA in the serum of AS rats increased significantly, and the activity of SOD and GSH-Px decreased significantly (P0.01). Compared with the AS rats, AS+ALCAR group rats significantly reduced the serum MDA concentration in AS rats and increased the serum inflammation in the rats. Compared with the control group, the content of serum TNF- a, IL-1 beta and CRP in the AS group increased significantly (P0.01). Compared with the AS group, the content of TNF- a, IL-1 beta and CRP decreased significantly in group AS+ALCAR (P0.01). Compared with the control group, the concentration of serum albumin in the rats of the group of AS groups was significantly lower than that in the control group. Change (P0.05).4. rat aorta histological examination: HE staining results showed that in the control group, the vascular lumen of the group ALCAR rats was larger, the wall of the tube was thinner, the intima structure of the vessel was complete and smooth, the smooth smooth muscle cells of the middle membrane were arranged, the lumen in the.AS group of the internal elastic membrane was narrower, the wall of the tube thickened obviously, the endothelial cells fell off, the smooth muscle cells were large. There was a lot of disorder and atheromatous plaque formation. There was a large number of foam cells and lipid deposition in.AS+ALCAR group than that of AS group. The severity of plaque was much lower than that of AS group.5. rats. Compared with the control group, the concentration of MDA in the aorta tissue of the AS group was significantly higher, SOD and GSH-Px. Compared with the AS group, ALCAR significantly reduced the MDA concentration in the aorta of the AS rats and increased the content of Ang II in the aorta of SOD and GSH-Px (P0.01).6. rats: compared with the control group, the content of the aorta Ang II in the AS rats increased significantly. Compared with the group, ALCAR could significantly reduce the Ang II content of aorta (P0.05) in the aorta of AS rats and the Real-time QPCR detection of the inflammatory substances in the aorta of.7.: AS can lead to a significant increase in the relative expression of TNF- alpha, IL-1 beta and iNOS mRNA. Expression (P0.01). The expression of CRP, TNF- alpha, IL-1 beta and iNOS mRNA in the aorta of the control group and the ALCAR group had no significant difference (P0.05) Western blot detection in the.8. aorta tissue: AS could significantly induce the aorta tissue of the rat aorta. The expression of protein had a significant downregulation effect (P0.01). There was no significant difference in the expression of CRP, TNF- a, IL-1 beta and iNOS protein in the control group and the ALCAR group (P0.05).9. cardiac tissue oxidative stress substance: compared with the control group, the concentration of MDA in the cardiac tissue of the group AS rats was significantly increased and the SOD and GSH-Px activity decreased significantly. ALCAR significantly reduced the concentration of MDA in the cardiac tissue of AS rats and increased the detection of Real-time QPCR in SOD and GSH-Px activity (P0.05 or P0.01).10. cardiac tissue inflammatory substances: AS could lead to rat cardiac tissue CRP. S mRNA overexpressed CRP, TNF- alpha, IL-1 beta and iNOS mRNA in.ALCAR group, and had statistical significance (P0.01 or P0.05).11. cardiac tissue inflammatory substances. The expression of iNOS protein has a significant downregulation effect (P0.05 or P0.01). Conclusion: 1. in AS rats, ALCAR can modulate blood lipid, inhibit gene and protein expression of inflammatory factors, antioxidant stress, and regulate arterial renin angiotensin system to counter atherosclerotic.2. ALCAR can reduce the basis of inflammatory factors in cardiac tissue of AS rats The expression of protein and protein, increasing its antioxidant capacity, may be related to its anti coronary atherosclerosis and myocardial protection, and further mechanism study should be carried out. Second the clinical efficacy and antioxidation and anti-inflammatory effects of levocarnitine on unstable angina pectoris of coronary heart disease: To observe the instability of CHD in coronary heart disease The clinical effect, antioxidation and anti-inflammatory effects of the patients with angina pectoris, and further explore the mechanism of Levocarnitine in the treatment of coronary heart disease. Methods: Taking the Weifang People's Hospital as a sample source, the selected time period was from August 2012 to December 2013, and the hospital was selected to be hospitalized for chest pain or chest tightness in this period of cardiovascular medicine. The results of arteriography showed that at least one of the main coronary artery stenosis was more than 50%, and was consistent with the <2007 years of unstable angina pectoris made in 2011 ACC/AHA, the updating of the non segment elevation myocardial infarction diagnosis guide, the diagnosis of unstable angina pectoris, the diagnosis of unstable angina pectoris, and the compliance with the exclusion criteria of 115 patients. The control group was divided into two groups, the control group (n=55) was given conventional coronary drug therapy, and the treatment group (n=60) was given levocarnitine treatment (2G/d) intravenous drip on the basis of routine treatment, and the treatment was treated for 7 days and changed into oral 2G to 56 days. The changes of clinical symptoms, blood lipid distribution, general blood biochemical indexes, and monitoring drugs were observed before and after the treatment of two groups. The effects of GSH-Px, MDA, hs-CRP, IL-6 and TNF-a were measured before and after treatment to evaluate the clinical efficacy of levocarnitine on coronary heart disease unstable angina and its anti-inflammatory and antioxidant effects on patients with coronary heart disease. This study was analyzed by the statistical software SPSS 17 logarithms, such as measurement data, using a mean number of standards. In the form of poor (x + s), the control group was compared with the paired t test before and after treatment in the treatment group. After treatment, the control group was compared with the treatment group with independent sample t test for data analysis. For example, the x2 test.P0.05 showed significant statistical difference for the count data. Results: 1. follow up and clinical treatment. Comparison: there were 2 cases in the control group. There were 3 cases in the treatment group because of the loss of follow-up. There was no drug side reaction in the follow-up process. The total effective rate of the treatment group was 91.22% and the control group 84.91% had no statistical significance (x 2=0.53, P=0.41), but the significant efficiency treatment group was 47.37% significantly higher than the control group 24.53% (x 2=5.23, P=0.02), and the difference between the treatment group and the control group was 47.37%. The comparison of blood lipid in different groups of statistical significance (P0.05).2. two groups: there was no difference in the level of TC, TG, LDL-C and HDL-C before treatment (P0.05). The level of LDL-C in the control group was significantly lower than before the treatment (P0.01), and the HDL-C level was not significantly changed (P0.05), and the level of the treatment group was significantly lower than before treatment. The level of HDL-C had a rising trend (P0.05). The level of TG in the treatment group was more obvious than that of the control group (1.65 + 0.21 mmol/L vs 1.79 + 0.10 mmol/L P0.01), and the level of HDL-C was significantly higher than that of the control group (1.02 + 0.26 mmol / L vs 0.89 + 0.41 mmol/L). Comparison of antioxidant capacity in group 2.55 + 1.06mmol/L vs 2.85 + 0.90 mmol/L P=0.11).3. two: there was no difference between the two groups before treatment (P0.05), the comparison of GSH-Px, MDA in the two groups before and after treatment. The two groups before and after treatment were significantly higher than those before the treatment and MDA obviously descended (P0.01), and the treatment group was higher than the control group after treatment. The decrease was more obvious (149.80 + 28.40 U/mL vs 125.45 + 23.32 U/mL P0.01, 5.99 + 0.52 mmol/L vs 6.25 + 0.60 mmol/L P=0.02) in.4. two group, and there was no significant difference between the two groups before treatment and IL-6.TNF- alpha (P0.05). The treatment group decreased more after treatment than in the control group. It was significant (1.65 + 0.62mmol/L vs 2.25 + 0.70mmol/L P0.01; 90.93 + 18.13 ng/L vs 115.82 + 17.50 ng/L P0.01; 11.85 + 2.85 pmol/L vs 13.25 + 3.17 pmol/L P=0.02), with statistical significance. Conclusion: levocarnitine has a definite effect on improving the symptoms of coronary heart disease unstable angina, and further on the basis of conventional medicine treatment It can relieve the clinical symptoms, improve the distribution of blood lipid, improve the activity of antioxidant enzymes, improve the ability of antioxidation, reduce the reaction of lipid peroxidation, reduce the inflammatory reaction, and treat atherosclerosis, thus treating coronary heart disease.

【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R543.5;R541.4

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