本文選題：視神經(jīng)損傷 + 內(nèi)皮祖細(xì)胞��； 參考：《天津醫(yī)科大學(xué)》2011年碩士論文

【摘要】：目的： 1。建立Wistar大鼠外傷性視神經(jīng)損傷動(dòng)物模型,探討不同損傷程度大鼠外傷性視神經(jīng)損傷后外周血內(nèi)皮祖細(xì)胞(endothelial progenitor cells,EPCs)的變化趨勢(shì)及其與白細(xì)胞、血小板變化的關(guān)系。 2.分析外傷性視神經(jīng)損傷對(duì)外周血內(nèi)皮祖細(xì)胞的影響。 3.探討內(nèi)皮祖細(xì)胞在外傷性視神經(jīng)損傷中的作用,為治療外傷性視神經(jīng)損傷提供理論依據(jù)。 方法： 1.采用液壓沖擊顱腦損傷儀建立外傷性視神經(jīng)損傷動(dòng)物模型,實(shí)驗(yàn)大鼠隨機(jī)分為視神經(jīng)損傷組(n=60)及正常對(duì)照組(n=20)；視神經(jīng)損傷組依據(jù)打擊力度不同分為輕度打擊組(n=20),中度打擊組(n=20),重度打擊組(n=20)三個(gè)亞組。觀察各組損傷前24h及損傷后3h、12h、24h、48h、72h、lw、2w、3w外周血EPCs、白細(xì)胞及血小板數(shù)量變化,同時(shí)觀察HE染色變化。 2.采用液壓沖擊顱腦損傷儀制作外傷性視神經(jīng)損傷動(dòng)物模型,實(shí)驗(yàn)大鼠隨機(jī)分為視神經(jīng)損傷組和正常對(duì)照組；兩組按照損傷前24h及損傷后3h、12h、24h、48h、72h、1w、2w、3w時(shí)間點(diǎn)隨機(jī)分為9個(gè)亞組。測(cè)定各組上述時(shí)間點(diǎn)外周血EPCs數(shù)量并觀察血管內(nèi)皮標(biāo)志物CD31免疫組化染色及F-VEP變化及微血管生成情況。 結(jié)果： 1.正常大鼠外周血EPCs數(shù)量為(46-52)個(gè)/20萬(wàn)單個(gè)核細(xì)胞,外傷性視神經(jīng)損傷后外周血EPCs于傷后12h達(dá)最低點(diǎn),各組間下降程度無(wú)顯著差異(F=0.496, P0.05);輕度打擊組及中度打擊組EPCs數(shù)量在傷后24-72h升高至正正常水平以上,于傷后72h達(dá)峰,此后逐漸下降至正常水平；重度打擊組EPCs于傷后24-72h雖有上升趨勢(shì),但達(dá)不到正正常水平；視神經(jīng)損傷后大鼠外周血中EPCs數(shù)量變化與白細(xì)胞及血小板的數(shù)量無(wú)顯著相關(guān)性(r=0.027,0.032,P0.05)。 2.正正常大鼠視神經(jīng)及周?chē)M織CD31+細(xì)胞數(shù)為(7-9)個(gè)／5個(gè)高倍視野,視神經(jīng)損傷后各時(shí)間點(diǎn)創(chuàng)傷區(qū)CD31+細(xì)胞計(jì)數(shù)分別為(8.36±1.52、7.17±1.10、10.41±1.92、11.43±1.58.14.29±2.03、17.33±1.47、17.86±1.22、18.13±1.40)個(gè)／5個(gè)高倍視野,視神經(jīng)損傷組與對(duì)照組比較,48h、72 h、1w、2w、3w時(shí)間點(diǎn)差異均有統(tǒng)計(jì)學(xué)意義(t=4.31,-7.61,-8.17,-10.08,-10.79;P0.05).正常大鼠視神經(jīng)及周?chē)M織微血管數(shù)量為(6～9)個(gè)/5個(gè)高倍視野,視神經(jīng)損傷后各時(shí)間點(diǎn)損傷區(qū)微血管數(shù)量分別為(6.52±1.05.7.54±2.01.8.52±2.21. 11.02±1.62.15.40±2.04.18.39±1.96.23.21±1.50.22.78±2.40.24.13±2.51)個(gè)/5個(gè)高倍視野,視神經(jīng)損傷組與對(duì)照組比較,48h.72 h.1w.2w.3w時(shí)間點(diǎn)差異均有統(tǒng)計(jì)學(xué)意義(t=4.25,-7.74,-8.26,-10.28,-11.49;P0.05).視神經(jīng)損傷后各時(shí)間點(diǎn)F-VEP中P波潛伏期于損傷后3h降低,24h反彈增高到正常水平以上,并趨于穩(wěn)定,視神經(jīng)損傷組與對(duì)照組相比,3h.12h.24h. 48h.72h.1w.2w.3w差異均有統(tǒng)計(jì)學(xué)意義(t=4.15,3.74,5.84,6.08, 6.40,6.52,6.53,6.61；P0.05)；F-VEP中振幅于3h降低,12h升高到接近基礎(chǔ)水平,24h后逐漸降低至基礎(chǔ)水平以下,實(shí)驗(yàn)組與對(duì)照組比較,3h、24h.48h.72h.1w.2w.3w差異有統(tǒng)計(jì)學(xué)意義(t=3.95,4.14,5.26,5.78,6.49,6.72,6.23;P0.05)。外周血內(nèi)皮祖細(xì)胞的數(shù)量變化與創(chuàng)傷區(qū)周?chē)鶦D31+細(xì)胞、微血管、F-VEP潛伏期及振幅變化存在相關(guān)性(r=0.43,0.41,0.43,0.47；P0.05)。 結(jié)論： 1.外傷性視神經(jīng)損傷大鼠外周血EPCs存在先降低后增高,再逐漸降至正常水平的變化特征。視神經(jīng)損傷越嚴(yán)重,EPCs增高幅度越小。 2.外傷性視神經(jīng)損傷能刺激外周血EPCs增加。 3.外傷性視神經(jīng)損傷后增加的外周血EPCs定向歸巢到創(chuàng)傷區(qū),參與了創(chuàng)傷區(qū)血管新生和組織損傷修復(fù)。
[Abstract]:Purpose :

1 . To establish an animal model of traumatic optic nerve injury in Wistar rats . The changes of endothelial progenitor cells ( EPCs ) after traumatic optic nerve injury in rats with different degree of injury were investigated .

2 . To analyze the effect of traumatic optic nerve injury on endothelial progenitor cells in peripheral blood .

3 . To investigate the role of endothelial progenitor cells in traumatic optic nerve injury and to provide theoretical basis for the treatment of traumatic optic nerve injury .

Method :

1 . An animal model of traumatic optic nerve injury was established by hydraulic percussion brain injury instrument . The experimental rats were randomly divided into optic nerve injury group ( n = 60 ) and normal control group ( n = 20 ) .
The changes of EPCs , white blood cells and platelets in peripheral blood at 3h , 12h , 24h , 48h , 72h , lw , 2w , 3w were observed at 3h , 12h , 24h , 48h , 72h , lw , 2w , 3w before and after injury , and the changes of HE staining were observed .

2 . The experimental rats were randomly divided into optic nerve injury group and normal control group .
Two groups were randomly divided into 9 subgroups according to 24 h before injury and 3 h , 12 h , 24 h , 48 h , 72 h , 1 w , 2w , and 3w time points .

Results :

1 . The number of EPCs in peripheral blood of normal rats was ( 46 - 52 ) / 200,000 mononuclear cells . After traumatic optic nerve injury , the EPCs of peripheral blood reached the lowest point after injury ( F = 0.496 , P0.05 ) .
In severe attack group , the EPCs tended to increase in 24 - 72 h after injury , but reached normal level .
There was no significant correlation between the number of EPCs and the number of white blood cells and platelets in the peripheral blood of rats after optic nerve injury ( r = 0.027 , 0.032 , P0.05 ) .

2 . The number of CD31 + cells in optic nerve and peripheral tissues of normal rats was ( 7.17 鹵 1.10 , 10.41 鹵 1.92 , 11.43 鹵 1.58.14 . 29 鹵 2 . 03 , 17.33 鹵 1 . 47 , 17.86 鹵 1.22 , 18.13 鹵 1.40 ) . The number of microvessels in the optic nerve and surrounding tissues of the normal rats was ( 6 - 9 ) / 5 high - fold visual field , and the number of microvessels at each time point after optic nerve injury was ( 6.52 鹵 1.05 . 7.54 鹵 2.01 . 8.52 鹵 2 . 21.11 . 02 鹵 1 . 96.23 . 21 鹵 1 . 50.22 . 78 鹵 1 . 96.23 . 21 鹵 1 . 50 . 22 . 78 鹵 2 . 40 . 24 . 13 鹵 2 . 51 ) / 5 high - fold field of view , and the difference in the time point of optic nerve injury was significantly different from that of the control group ( t = 4.25 , - 7.74 , - 8.26 , - 10.28 , - 11.49 ; P0.05 ) . The latency of P wave in F - VEP after optic nerve injury was decreased at 3 h after injury , and the rebound increased to above normal level at 24 h , and tended to be stable . The difference of optic nerve injury group and control group was significantly ( t = 4.15 , 3.74 , 5.84 , 6.08 , 6.40 , 6.52 , 6.53 , 6.61 ) .
P0.05)錛，

本文編號(hào)：1808252