【摘要】：背景:異常應(yīng)力被認(rèn)為是導(dǎo)致椎間盤退變的重要因素。隨著對椎間盤退變發(fā)生機制研究的不斷深入,建立一種理想的力學(xué)相關(guān)性椎間盤退變體內(nèi)動物模型具有重要的實踐意義。目的:建立兔椎間盤體內(nèi)模型,施以持續(xù)的張力載荷,探究其對椎間盤退變的影響。方法:25只6月齡新西蘭大白兔隨機分為3組,空白對照組5只,假加力組10只,加力組10只�？瞻讓φ战M不作任何處理,于實驗第1天手術(shù)獲取L_(4/5)椎間盤;加力組和假加力組均固定椎間盤加力器,加力組施以L_(4/5)椎間盤1 MPa(10 kg/cm~2)軸向牽張力,假加力組僅固定加力器但不加力,2組分別在14,28 d手術(shù)獲取椎間盤。X射線觀察L_(4/5)椎間隙高度變化和鄰近骨質(zhì)改變;蘇木精-伊紅染色觀察椎間盤組織形態(tài)學(xué)變化;NBT染色觀察椎間盤細(xì)胞存活狀態(tài);RT-PCR檢測各時間點椎間盤組織中蛋白聚糖、Ⅱ型膠原和SOX9 m RNA表達(dá)變化。結(jié)果與結(jié)論:(1)假加力組各時間點與空白對照組相比,X射線表現(xiàn)、蘇木精-伊紅染色、細(xì)胞存活狀態(tài)和蛋白多糖、Ⅱ型膠原、SOX9 m RNA表達(dá)差異均無顯著性意義;(2)與空白對照組相比發(fā)現(xiàn),加力組隨著張力載荷時間的延長,L_(4/5)椎間隙逐漸變窄,關(guān)節(jié)面毛糙,上下椎體前緣骨質(zhì)增生呈唇狀改變;椎間盤細(xì)胞分布不均勻、紊亂;髓核脫水縮小,纖維環(huán)排列混亂,脊索細(xì)胞空泡狀組織趨于消失;蛋白多糖、Ⅱ型膠原、SOX9表達(dá)顯著下調(diào);(3)結(jié)果提示,成功建立了兔椎間盤體內(nèi)模型,并在此模型基礎(chǔ)上闡明持續(xù)張力載荷可直接導(dǎo)致椎間盤退變。
[Abstract]:Background: abnormal stress is considered to be an important factor leading to disc degeneration. With the further study of the mechanism of disc degeneration, it is of great practical significance to establish an ideal animal model of intervertebral disc degeneration in vivo. Aim: to establish a model of intervertebral disc in rabbits and to investigate the effect of continuous tension load on the degeneration of intervertebral disc. Methods Twenty five 6 months old New Zealand white rabbits were randomly divided into 3 groups: blank control group (n = 5), sham exertion group (n = 10) and postconditioning group (n = 10). The blank control group received L4 / 5 intervertebral disc without any treatment on the first day of the experiment, and the L _ (4 / 5) intervertebral disc axial tension of 1 MPa (10 kg/cm~2) was applied to the control group. In the sham exertion group, the height of L4 / 5 intervertebral space and the changes of adjacent bone were observed at 1428 d after operation. Histomorphologic changes of intervertebral disc were observed by hematoxylin and eosin staining. The expression of proteoglycan, type 鈪，

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