本文選題：成纖維細(xì)胞生長(zhǎng)因子受體　切入點(diǎn)：失神經(jīng)　出處：《蘭州大學(xué)》2017年碩士論文

【摘要】：目的成纖維細(xì)胞生長(zhǎng)因子受體3是是酪氨酸家族里面位于細(xì)胞膜表面的一種膜蛋白,在參于組織修復(fù)、信號(hào)傳導(dǎo)、細(xì)胞再生分化、凋亡中發(fā)揮著重要作用。大量國(guó)內(nèi)外研究發(fā)現(xiàn),成纖維細(xì)胞生長(zhǎng)因子受體3是成纖維細(xì)胞生長(zhǎng)因子家族里唯一一個(gè)負(fù)向調(diào)控骨骼代謝。在臨床中某些遺傳病如軟骨發(fā)育不全(ACH)、季肋發(fā)育不全(HCH)和致死性骨發(fā)育不全(TD)等都與FGFR3基因突變有關(guān)。而在失神經(jīng)骨折愈合中,FGFR3的報(bào)道甚少。并且在大鼠失神經(jīng)骨折愈合過程中產(chǎn)生的骨痂是病理性骨痂,強(qiáng)度差,密度分布不均勻,本實(shí)驗(yàn)研究FGFR3與失神經(jīng)骨痂的關(guān)系。通過建立失神經(jīng)骨折模型并給予注射FGFR3抑制劑,觀察骨痂生成過程中鈣鹽沉積速率。探討該受體與失神經(jīng)骨折愈合過程中骨痂礦化的關(guān)系以及骨吸收和骨折愈合之間的關(guān)系。為如何改善脊髓損傷后骨質(zhì)的流失及骨痂的礦化提供一個(gè)理論依據(jù)。方法本研究將96只成年健康雌性wistar大鼠隨機(jī)分為實(shí)驗(yàn)組和對(duì)照組。實(shí)驗(yàn)組建立T10脊髓離斷下的脛骨骨折模型,并于術(shù)后給予FGFR3阻滯劑;對(duì)照組為T10脊髓離斷合并脛骨骨折模型,術(shù)后給予等劑量生理鹽水,分別于術(shù)后第7、14、21、28天取標(biāo)本(每個(gè)時(shí)間點(diǎn)=10只),經(jīng)固定、脫鈣處理后,在骨折端上下5 mm處修剪標(biāo)本,石蠟包埋,切成6μm切片。切片應(yīng)用于臧紅固綠染色、masson三色染色。并分別于術(shù)后7、14、21、28天拍X片、骨痂骨密度測(cè)定,另每組另外8只大鼠用于鈣黃綠素雙標(biāo)實(shí)驗(yàn),并做硬組織切片,行VG染色。結(jié)果失神經(jīng)后實(shí)驗(yàn)組骨痂骨密度較對(duì)照組相比,骨痂骨密度明顯增高,具有統(tǒng)計(jì)學(xué)差異(p0.05)。雙熒光標(biāo)記寬度實(shí)驗(yàn)組較對(duì)照組明顯增寬(p0.05)。影像學(xué)顯示實(shí)驗(yàn)組骨折愈合速度明顯高于對(duì)照組,并且在組織學(xué)方面提示不同時(shí)間點(diǎn)實(shí)驗(yàn)組在骨折愈合進(jìn)程加速。結(jié)論FGFR3參與大鼠失神經(jīng)后骨折愈合過程中骨痂的礦化過程,負(fù)性調(diào)節(jié)骨痂的礦化,在骨折愈合塑性重建中發(fā)揮重要作用。
[Abstract]:A large number of domestic and foreign studies have found that fibroblast growth factor receptor 3 is the only negative regulation of bone metabolism in the fibroblast growth factor family.In clinic, some hereditary diseases, such as chondroplasia, FGFR3) and fatal bone dysplasia, are associated with FGFR3 gene mutation.FGFR 3 was rarely reported in the healing of denervated fractures.The callus produced during the healing of denervated fracture in rats was pathological callus with poor strength and uneven density distribution. This study was conducted to study the relationship between FGFR3 and denervated callus.The calcium deposition rate during callus formation was observed by establishing denervated fracture model and injecting FGFR3 inhibitor.To investigate the relationship between the receptor and callus mineralization in the healing of denervated fractures and the relationship between bone resorption and fracture healing.To provide a theoretical basis for improving bone loss and callus mineralization after spinal cord injury.Methods 96 adult female wistar rats were randomly divided into experimental group and control group.The experimental group established tibial fracture model with T10 spinal cord fracture and was treated with FGFR3 blocker after operation, while the control group was treated with normal saline at the same dose after operation, while the control group was treated with T10 spinal cord fracture with tibial fracture.The sections were applied to Zang Hong solid green staining and mass on three color staining.The bone mineral density of callus was measured at 28 days after operation. The other 8 rats in each group were used for calcitonin double labeling test, hard tissue sections and VG staining.Results the bone mineral density of callus in the experimental group after denervation was significantly higher than that in the control group (P 0.05).The width of double fluorescence labeling in the experimental group was significantly wider than that in the control group.Imaging showed that the fracture healing speed in the experimental group was significantly higher than that in the control group, and histologically, the healing process of the experimental group was accelerated at different time points.Conclusion FGFR3 is involved in the mineralization of callus in the healing process of denervated fracture in rats, and plays an important role in plastic reconstruction of fracture healing.
【學(xué)位授予單位】：蘭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R651.2;R683

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