發(fā)布時(shí)間：2018-07-17 17:48

【摘要】：[目的]1.利用異氟烷麻醉方法和下腔靜脈狹窄法構(gòu)建DVT機(jī)化再通模型；使用血紅素加氧酶-1的激動(dòng)劑(CoPPIX)及抑制劑(SnPPIX)干預(yù)C57小鼠DVT的溶解再通過程,并觀察各組小鼠DVT模型的死亡率、成栓率,下腔靜脈血栓的長(zhǎng)度、濕重和病理切片的變化差異。2.檢測(cè)C57小鼠下腔靜脈壁和血栓的HO-1、VEGF和SDF-1的表達(dá)情況,探討HO-1、 VEGF和SDF-1在DVT溶解中后期的作用及相互關(guān)系。[材料與方法]實(shí)驗(yàn)一：下腔靜脈狹窄法構(gòu)建C57小鼠DVT模型及觀察HO-1激動(dòng)劑及抑制劑對(duì)DVT機(jī)化再通過程的影響1.實(shí)驗(yàn)分組及DVT模型的構(gòu)建：C57小鼠200只,體重25-30g,雌性。按隨機(jī)分組原則分A組(空白對(duì)照組,n=20)、B組(正常DVT組,n=60)、C組(CoPPIX干預(yù)組,n=60)組和D組(SnPPIX干預(yù)組,n=60)。C組和D組在造模前24h分別腹腔注射CoPPIX和SnPPXI,5mg/kg; B組腹腔注射等量的生理鹽水。給藥24小時(shí)后B、C、D采用異氟烷麻醉配合下腔靜脈狹窄法構(gòu)建DVT模型。2.取材：在造模后4、7、10、13天,采取頸椎脫臼法處死小鼠,采用游標(biāo)卡尺測(cè)量血栓長(zhǎng)度,取下結(jié)扎點(diǎn)至髂總靜脈匯合處之間下腔靜脈及其內(nèi)容物,每個(gè)時(shí)間點(diǎn)每組中隨機(jī)取3只小鼠DVT標(biāo)本,使用4%多聚甲醛浸泡固定,保存行病理檢查；其余標(biāo)本分離血栓與靜脈壁,稱取血管內(nèi)的血栓濕重,靜脈壁和內(nèi)容物分裝后-80°保存?zhèn)溆谩?.指標(biāo)測(cè)定和統(tǒng)計(jì)學(xué)分析：統(tǒng)計(jì)每組死亡率、成栓率、血栓長(zhǎng)度和濕重變化情況。統(tǒng)計(jì)學(xué)軟件采用SPSS19.0,計(jì)量資料采用均數(shù)±標(biāo)準(zhǔn)差(x±s)；同一時(shí)間點(diǎn),組間兩兩比較采用單因素方差分析、用LSD法(最小二乘法),*p0.05有統(tǒng)計(jì)學(xué)意義。實(shí)驗(yàn)二：不同時(shí)間點(diǎn)各組小鼠DVT模型靜脈壁組織中HO-1、VEGF和SDF-1的mRNA達(dá)變化1.Trizol法提取每組小鼠不同時(shí)間點(diǎn)下腔靜脈中總RNA, RT-PCR將各組小鼠靜脈組織RNA逆轉(zhuǎn)錄為cDNA;以GAPDH為內(nèi)參照,用Real-time PCR法檢測(cè)不同時(shí)間點(diǎn)HO-1、VEGF和SDF-1 mRNA的表達(dá)變化；2.統(tǒng)計(jì)學(xué)分析：統(tǒng)計(jì)學(xué)軟件采用SPSS19.0o計(jì)量資料采用均數(shù)±標(biāo)準(zhǔn)差(x±s)；同一時(shí)間點(diǎn),組間兩兩比較采用單因素方差分析,用LSD法(最小二乘法),*p0.05有統(tǒng)計(jì)學(xué)意義。[結(jié)果]實(shí)驗(yàn)一：下腔靜脈狹窄法構(gòu)建C57小鼠DVT模型及觀察HO-1激動(dòng)劑及抑制劑對(duì)DVT機(jī)化再通過程的影響1.麻醉效果：實(shí)驗(yàn)開始使用3%-5%異氟烷對(duì)C57小鼠進(jìn)行快速誘導(dǎo),術(shù)中使用0.5%-1.0%濃度的異氟烷能維持滿意的麻醉效果。誘導(dǎo)達(dá)到麻醉滿意時(shí)間和術(shù)后清醒時(shí)間均很快,約1-2min,麻醉過程中小鼠出現(xiàn)的最大不良反應(yīng)為呼吸抑制,但停止麻醉藥或加大空氣流量后,小鼠呼吸抑制的情況可迅速緩解.2.小鼠存活情況和死亡率：A、D兩組死亡率為0%,B、C兩組總死亡率分別為1.67%3.各組模型的總成栓率：A組小鼠成栓率為0%,B、C、D組總成栓率分別為69.4%、62.7%、83.3%4.不同時(shí)間點(diǎn)各組模型中的DVT長(zhǎng)度變化情況：各組的DVT長(zhǎng)度經(jīng)單因素方差分析比較后顯示：第4天時(shí),C組、D組的DVT長(zhǎng)度和B組相比無明顯統(tǒng)計(jì)學(xué)差異,但C組與D組之間比較時(shí)P=0.018,P0.05,兩組之間存在統(tǒng)計(jì)學(xué)差異；第7天時(shí),B、C、D各組間兩兩比較無統(tǒng)計(jì)學(xué)差異；第10天時(shí),C、D組的DVT長(zhǎng)度和正常組相比無明顯統(tǒng)計(jì)學(xué)差異, C組與D組之間比較時(shí)P=0.003,P0.05,兩組之間存在統(tǒng)計(jì)學(xué)差異；第13天時(shí),B、C、D各組間兩兩比較均存存明顯的統(tǒng)計(jì)學(xué)差異,尤其是C組和D組之間,P0.001。最后,該實(shí)驗(yàn)比較了各組第4天到第13天的DVT長(zhǎng)度的平均值減少比例,結(jié)果顯示,B、C、D組DVT長(zhǎng)度平均減少量分別為2.19mm、2.74mm、2.16mm,各組的減少比例分別為37.6%、49.5%和31.9%。5.不同時(shí)間點(diǎn)各組模型中的DVT濕重變化情況：各組的DVT濕重經(jīng)單因素方差分析比較后顯示：第4天時(shí),B、C組之間無明顯統(tǒng)計(jì)學(xué)差異,P=0.719,但B、C組與D組之間存在明顯統(tǒng)計(jì)學(xué)差異,P值分別為0.013和0.01,均小于0.05；第7天時(shí),B組與C、D組之間比較無統(tǒng)計(jì)學(xué)差異,而C組和D組之間比較,P=0.019,兩組之間DVT濕重存在明顯統(tǒng)計(jì)學(xué)差異；第10天時(shí),B組和C組之間無明顯統(tǒng)計(jì)學(xué)差異,P=0.365,B、C組與D組之間存在明顯統(tǒng)計(jì)學(xué)差異,P值分別為0.008和0.001,第13天時(shí),第13天時(shí)B、C、D組之間兩兩比較均存在明顯的統(tǒng)計(jì)學(xué)差異,P值均0.001。最后,該實(shí)驗(yàn)比較了了各組第4天到第13天的DVT濕重的平均值減少比例,結(jié)果顯示,B、C、D組DVT濕重平均減少量分別為7.1mg、8.14mg、6.2mg,各組的減少比例分別為55.5%、72.0%和41.1%。6.各組各時(shí)間點(diǎn)的DVT病理學(xué)改變：A組中均未見DVT形成。B、C、D分別于術(shù)后第7、10、13天取材,有DVT形成小鼠的下腔靜脈內(nèi)可見紅白相間的固體質(zhì)塊,即血栓,且隨著術(shù)后飼養(yǎng)的時(shí)間推移,DVT的長(zhǎng)度逐漸變短,直徑也逐漸變細(xì)。切片行HE染色后在顯微鏡下可見：隨著時(shí)間推移,各組DVT機(jī)化面積逐漸曾加,機(jī)化的血栓邊緣與血管壁之間存在粘連。第13天時(shí)可見,C組DVT已全部機(jī)化,并且可見DVT內(nèi)有血管樣結(jié)構(gòu)形成,且可見機(jī)化區(qū)域有大量的裂隙產(chǎn)生；C組與B組相比,DVT內(nèi)炎癥細(xì)胞明顯較少,且B組可見DVT機(jī)化面積已經(jīng)超過橫截面積的一半,而D組其DVT機(jī)化面積明顯較小,機(jī)化面積僅接近DVT橫截面積的一半。實(shí)驗(yàn)二：不同時(shí)間點(diǎn)各組小鼠DVT模型靜脈壁組織中HO-1、VEGF和SDF-1的mRNA表達(dá)變化PCR結(jié)果以A組為空白對(duì)照組,檢測(cè)各組HO-1、VEGF和SDF-1的mRNA的相對(duì)表達(dá)量,結(jié)果經(jīng)統(tǒng)計(jì)學(xué)分析后得出,在DVT形成后第4、7、10、13天,B、C、D組的HO-1的表達(dá)均存在顯著統(tǒng)計(jì)學(xué)差異,兩兩之間比較,P0.05；相應(yīng)的,第4、7、10天VEGF的表達(dá)也均存在統(tǒng)計(jì)學(xué)差異,P0.05,第13天時(shí)B、C組之間無統(tǒng)計(jì)學(xué)差異,P0.05,B、C與D組之間比較P0.05,存在統(tǒng)計(jì)學(xué)差異；第4、7、10、13天,B、C、D組的SDF-1的表達(dá)均存在顯著統(tǒng)計(jì)學(xué)差異,兩兩之間比較,P0.05。[結(jié)論]1.異氟烷在小鼠麻醉過程中安全有效,誘導(dǎo)快,復(fù)蘇快,不增加動(dòng)物模型死亡率。2.下腔靜脈狹窄法能夠?qū)崿F(xiàn)DVT機(jī)化再通模型的構(gòu)建；3.HO-1在血栓形成過程中具有保護(hù)作用；在DVT溶解中后期HO-1可能通過誘導(dǎo)VEGF和SDF-1高表達(dá)促進(jìn)DVT再通。
[Abstract]:[Objective]1. to construct the DVT repass model by isoflurane anesthesia and inferior vena cava stenosis method; use the heme oxygenase -1 agonist (CoPPIX) and inhibitor (SnPPIX) to intervene the dissolution and repassage process of DVT in C57 mice, and observe the mortality, thrombus rate, the length of inferior vena cava thrombus, wet weight and pathological section of the mice DVT model in each group. The variation of.2. in the inferior vena cava and thrombus in C57 mice was detected by.2., and the expression of VEGF and SDF-1 were detected. The effect and relationship of HO-1, VEGF and SDF-1 in the middle and late stages of DVT dissolution. [materials and methods] Experiment 1: the inferior vena cava stenosis method was used to construct DVT model of C57 mice and observe HO-1 agonists and inhibitors. 1. experimental group and DVT model were constructed: 200 C57 mice, weight 25-30g, female. According to the principle of random grouping, A group (blank control group, n=20), group B (normal DVT group, n=60), C group (CoPPIX intervention group, n=60) group and D group The same amount of physiological saline. After 24 hours of administration, B, C, D used isoflurane anesthesia combined with the inferior vena cava stenosis method to construct DVT model.2. material: after 4,7,10,13 days after the model, the cervical dislocations were taken to kill the mice, the vernier caliper was used to measure the thrombus length, and the inferior vena cava and its contents between the ligation point and the general iliac vein were taken down, each time was taken. 3 DVT specimens of mice in each group were randomly selected to be soaked with 4% polyformaldehyde and preserved for pathological examination. The remaining specimens were separated from the thrombus and venous wall, and the thrombus was weighed in the blood vessels. The venous wall and the contents of the contents were measured and analyzed by the.3. index of -80 degrees after the separation of the venous walls and contents: the mortality, the thrombus rate, the length of thrombus and the length of the thrombus were statistically analyzed. The change of wet weight. The statistical software used SPSS19.0, the measurement data used mean standard deviation (x + s); the same time point, 22 comparison between the groups using single factor analysis of variance, the LSD method (least square method), *p0.05 has statistical significance. Experiment two: HO-1, VEGF and SDF-1 mRNA in the DVT model of each group of mice at different time points. The 1.Trizol method was used to extract the total RNA in the inferior vena cava of each group of mice at different time points, and RT-PCR was used to reverse the reverse transcription of RNA in each group of mice to cDNA, and GAPDH as the internal reference. The Real-time PCR method was used to detect the changes of HO-1, VEGF and SDF-1 mRNA at different time points. Statistical analysis was used for statistical analysis. Mean standard deviation standard deviation (x + s); the same time point, 22 comparison between groups using single factor analysis of variance, LSD method (least square method), *p0.05 has statistical significance. [results] Experiment 1: inferior vena cava stenosis method to construct DVT model of C57 mice and observe the effect of HO-1 agonist and inhibitor on DVT mechanical repassage process of DVT: 1. anesthesia effect: experimental opening 3%-5% isoflurane was used for rapid induction of C57 mice. The 0.5%-1.0% concentration of isoflurane could maintain a satisfactory anesthetic effect. The induction of anesthesia satisfaction time and postoperative waking time were very fast, about 1-2min. The biggest adverse reaction in the anesthetic process was repression, but stopped anaesthetized or increased air flow. After the respiratory inhibition, the survival and mortality of.2. mice were quickly relieved: the mortality of A, D two groups was 0%, B, and the total mortality of C two groups was the total thrombus rate of each group of 1.67%3. models, respectively: the thrombus rate of the A group was 0%, B, C, and D group was 69.4%, 62.7%, and 83.3%4. in the different time points of each group were changed to the length of DVT length. Condition: the DVT length of each group was compared with the single factor analysis of variance. At fourth days, there was no significant difference in the length of DVT in group C and group D compared with B group, but there was a statistical difference between the C group and the D group in P=0.018, P0.05 and two groups; at seventh days, B, C, and there was no statistical difference between the groups of D, and tenth days. There was no significant difference in length compared with the normal group. There was a statistical difference between group C and group D, P=0.003, P0.05, and two groups. At thirteenth days, B, C, and D were statistically different among 22 groups, especially between the C group and the D group, P0.001. last, and the experiment compared the DVT length of each group from fourth to thirteenth days. The average decrease in the mean value of the B, C and D groups was 2.19mm, 2.74mm, 2.16mm, respectively, and the decrease ratio of each group was 37.6%, 49.5% and 31.9%.5. at different time points, respectively. The wet weight of DVT in each group of different time points of each group showed that the wet weight of DVT in each group was compared with one factor analysis of variance: fourth days, B, no obvious series between C groups. There were significant differences in P=0.719, but there were significant statistical differences between B, C group and D group, P value was 0.013 and 0.01, respectively less than 0.05. At seventh days, there was no statistical difference between group B and C, D group, and C group and D group, P=0.019, there was significant difference between the two groups. Tenth days, there was no significant statistics between the group and the group. There were significant differences between P=0.365, B, C group and D group, P values were 0.008 and 0.001 respectively. At thirteenth days, thirteenth days, B, C, D groups were all statistically significant differences, and P values were all 0.001. last. The experiment compared the average value of DVT wet weight in each group from fourth days to thirteenth days. The average decrease in wet weight of VT was 7.1mg, 8.14mg, 6.2mg. The reduction ratio of each group was 55.5%, 72% and 41.1%.6. in each group. The DVT pathological changes of each time point were found in group A: no DVT formed.B, C, D were taken from the postoperative 7,10,13 days respectively. With the passage of time after operation, the length of DVT gradually became shorter and the diameter was gradually thinning. The slice line HE staining was visible under the microscope: as time went on, the area of DVT in each group gradually increased, and there was a adhesion between the edge of the thrombus and the wall of the blood vessel. The DVT of group C was all computerized in the thirteenth day, and there was a vascular like in DVT. The structure was formed, and there was a large number of cracks in the visible area. Compared with the B group, the C group was obviously less inflammatory cells in DVT, and the area of DVT in the B group was more than half of the cross section area, while the DVT area of the D group was smaller and the area was only half of the DVT cross section. Experiment two: mice DVT at different time points. The mRNA expression changes of HO-1, VEGF and SDF-1 in the venous wall tissue of the model were compared with the A group as the blank control group, and the relative expression of HO-1, VEGF and SDF-1 mRNA in each group was detected. The results were statistically analyzed after statistical analysis, and there were significant differences in the expression of the 4,7,10,13 days after the formation of DVT. 22 Correspondingly, there were statistical differences in the expression of VEGF in day 4,7,10. P0.05, B at thirteenth days, there was no statistical difference between group C and P0.05, B, C and D, and there were significant statistical differences between P0.05, C and D group. In the process of intoxication, it is safe, effective, fast inducement, rapid recovery, no increase of animal model mortality,.2. inferior vena cava stenosis method can realize the construction of DVT repass model, 3.HO-1 has protective effect in the process of thrombosis, and HO-1 may promote DVT repass by inducing the high expression of VEGF and SDF-1 in the middle and late stages of DVT dissolution.
【學(xué)位授予單位】：昆明醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R543.6

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2 唐興榮;張水冰;余尚貞;;腦立蘇顆粒對(duì)急性腦缺血大鼠腦組織HO-1表達(dá)的影響[A];第八次全國(guó)中西醫(yī)結(jié)合虛證與老年醫(yī)學(xué)學(xué)術(shù)研討會(huì)論文集[C];2005年

3 張錚;秦海東;沈華;徐英;馬明洲;程惠;宋希;鮑磊;;納絡(luò)酮對(duì)大鼠肺缺血再灌注損傷中細(xì)胞凋亡及HO-1表達(dá)的影響[A];中華醫(yī)學(xué)會(huì)急診醫(yī)學(xué)分會(huì)第十三次全國(guó)急診醫(yī)學(xué)學(xué)術(shù)年會(huì)大會(huì)論文集[C];2010年

4 卓鳳婷;薛耀明;關(guān)美萍;沙建平;魏民;鄒藝;曾展軍;;晚期糖基化終產(chǎn)物對(duì)健康成人外周血單核細(xì)胞TNF-α和HO-1表達(dá)的影響[A];2008中國(guó)醫(yī)師協(xié)會(huì)內(nèi)分泌代謝科醫(yī)師分會(huì)年會(huì)論文匯編[C];2008年

5 史紅陽;孫秀珍;劉原;李滿祥;;他汀類通過上調(diào)HO-1和p21的表達(dá)抑制肺動(dòng)脈平滑肌細(xì)胞增殖[A];中國(guó)生理學(xué)會(huì)第23屆全國(guó)會(huì)員代表大會(huì)暨生理學(xué)學(xué)術(shù)大會(huì)論文摘要文集[C];2010年

6 曹海軍;陳淼;;HO-1對(duì)ARDS大鼠肺泡Ⅱ型上皮細(xì)胞保護(hù)作用的研究進(jìn)展[A];貴州省醫(yī)學(xué)會(huì)重癥醫(yī)學(xué)分會(huì)第三屆學(xué)術(shù)年會(huì)論文匯編[C];2008年

7 柴其翔;王季石;韋四喜;王婭婷;;HO-1通過慢病毒調(diào)控K562-ADM耐藥細(xì)胞株逆轉(zhuǎn)耐藥及其機(jī)制研究[A];中國(guó)腫瘤內(nèi)科進(jìn)展 中國(guó)腫瘤醫(yī)師教育（2014）[C];2014年

8 黃賢珍;唐琴;楊亦彬;;HIF-1α及HO-1在糖尿病鼠腎組織的表達(dá)及意義[A];貴州省醫(yī)學(xué)會(huì)腎臟病學(xué)分會(huì)2008年學(xué)術(shù)年會(huì)論文匯編[C];2008年

9 李倩;武維恒;;辛伐他汀對(duì)缺氧復(fù)氧心肌細(xì)胞表達(dá)HO-1的影響及機(jī)制[A];第十三次全國(guó)心血管病學(xué)術(shù)會(huì)議論文集[C];2011年

10 段國(guó)辰;凌亦凌;谷振勇;韋鵬;牛志云;楊世方;;八肽膽囊收縮素抑制LPS誘導(dǎo)的主動(dòng)脈平滑肌細(xì)胞iNOS和HO-1基因的表達(dá)[A];第六次全國(guó)缺氧和呼吸病理生理學(xué)術(shù)會(huì)議論文摘要匯編[C];2003年

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1 吳錫階;HO-1轉(zhuǎn)基因治療對(duì)非協(xié)調(diào)性異種心臟移植物的影響[D];福建醫(yī)科大學(xué);2008年

2 蔣路平;阿托伐他汀及雷帕霉素對(duì)HO-1表達(dá)和血管平滑肌細(xì)胞增殖的影響研究[D];中南大學(xué);2007年

3 梁超;異丙酚及DMSO上調(diào)人臍靜脈內(nèi)皮細(xì)胞HO-1表達(dá)的實(shí)驗(yàn)研究[D];復(fù)旦大學(xué);2012年

4 胡建莉;飲酒、HO-1基因啟動(dòng)子微衛(wèi)星多態(tài)性與食管鱗癌易感性的關(guān)聯(lián)研究[D];華中科技大學(xué);2010年

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1 高潔;活性鹵酚化合物對(duì)血管內(nèi)皮細(xì)胞EA.hy926中HO-1的誘導(dǎo)及其上游信號(hào)通路的調(diào)控作用[D];山西醫(yī)科大學(xué);2015年

2 張斌;HO-1通過抑制Stat3對(duì)銀屑病的治療機(jī)制研究[D];南京大學(xué);2014年

3 俞美聲;HO-1高表達(dá)減輕急性移植物抗宿主病的作用及機(jī)制研究[D];貴州醫(yī)科大學(xué);2016年

4 董忠禮;HO-1誘導(dǎo)靜脈內(nèi)皮細(xì)胞VEGF、SDF-1表達(dá)促進(jìn)DVT機(jī)化再通的研究[D];昆明醫(yī)科大學(xué);2016年

5 王磊;HO-1激動(dòng)劑治療慢性非細(xì)菌性前列腺炎的研究[D];重慶醫(yī)科大學(xué);2011年

6 狄純嬋;HO-1與MIP-1β在冠狀動(dòng)脈粥樣硬化性心臟病中的表達(dá)及其相關(guān)性研究[D];延邊大學(xué);2011年

7 王淑云;HO-1在人非小細(xì)胞肺癌細(xì)胞和組織中的表達(dá)及其對(duì)VEGF的影響[D];山東大學(xué);2012年

8 孫海軍;慢病毒介導(dǎo)HO-1基因轉(zhuǎn)染對(duì)骨髓間充質(zhì)干細(xì)胞體外缺血性損傷保護(hù)作用的實(shí)驗(yàn)研究[D];蘇州大學(xué);2011年

9 張靜;糖脈通對(duì)早期糖尿病下肢血管病變的臨床干預(yù)及sRAGE、HO-1表達(dá)的研究[D];山東中醫(yī)藥大學(xué);2014年

10 徐貴森;大鼠脊髓缺血再灌注后HO-1表達(dá)的變化和意義及異丙酚的影響[D];第三軍醫(yī)大學(xué);2006年

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