本文選題：核心蛋白聚糖 + 聲帶瘢痕��； 參考：《山東中醫(yī)藥大學(xué)》2017年碩士論文

【摘要】：目的:構(gòu)建新西蘭兔聲帶損傷模型,在聲帶瘢痕形成的不同時(shí)期,于損傷部位周圍多方向外源性注入核心蛋白聚糖(Decorin,DCN),分析聲帶組織病理學(xué)改變和轉(zhuǎn)化生長(zhǎng)因子-β1(Transforming growth factor-β1,TGF-β1)表達(dá)變化,觀察DCN能否抑制聲帶瘢痕增生,探討DCN抑制瘢痕增生的作用機(jī)制。方法:選取新西蘭兔25只,隨機(jī)選取20只做雙側(cè)聲帶急性損傷模型,用喉鉗夾取雙側(cè)聲帶前中部組織。選取10只新西蘭兔立即進(jìn)行右側(cè)聲帶損傷部位周圍多方向注入100μg/L的核心蛋白聚糖,左側(cè)聲帶損傷部位作為對(duì)照聲帶(A組),其它10只于聲帶損傷1月后進(jìn)行右側(cè)聲帶損傷部位周圍多方向注入100μg/L的核心蛋白聚糖,左側(cè)聲帶損傷部位作為對(duì)照聲帶(B組),剩余5只新西蘭兔作為無(wú)干預(yù)對(duì)照組(C組)。A組、B組新西蘭兔于注射核心蛋白聚糖后4周、12周分別隨機(jī)挑選5只收獲聲帶組織。將3組新西蘭兔收獲的聲帶組織進(jìn)行HE染色和免疫組織化學(xué)染色,分析聲帶組織的病理學(xué)改變和TGF-β1表達(dá)變化,將各組所得值相對(duì)比并進(jìn)行統(tǒng)計(jì)學(xué)分析。結(jié)果:1、通過(guò)環(huán)甲膜切開(kāi)的方式損傷新西蘭兔的聲帶組織,成功完成了聲帶損傷動(dòng)物模型的構(gòu)建,為接下來(lái)研究外源性注入DCN能否抑制聲帶瘢痕增生奠定了基礎(chǔ)。2、HE染色結(jié)果新西蘭兔的無(wú)損傷聲帶組織可見(jiàn)明顯的分層構(gòu)造,依次為上皮層、固有層和肌層,固有層主要是松散的結(jié)締組織,膠原纖維的排列比較規(guī)則。聲帶損傷組可見(jiàn)聲帶固有層的纖維組織成分明顯增多,膠原纖維比較密集,排列也非常雜亂,染色比無(wú)損傷聲帶明顯加深。DCN注射組可見(jiàn)固有層纖維組織比無(wú)損傷聲帶有所增多,但膠原纖維的排列比較規(guī)則,染色比聲帶損傷組明顯變淺。3、免疫組織化學(xué)染色結(jié)果(1)A、B兩組比C組聲帶TGF-β1的陽(yáng)性表達(dá)高,有顯著的統(tǒng)計(jì)學(xué)意義。(P0.01)(2)A、B兩組右側(cè)聲帶比左側(cè)聲帶TGF-β1的陽(yáng)性表達(dá)明顯減少,差異有顯著統(tǒng)計(jì)學(xué)意義。(P0.01)(3)A組比B組TGF-β1的陽(yáng)性表達(dá)明顯減少,差異有統(tǒng)計(jì)學(xué)意義。(P0.01)(4)A、B兩組,12周后觀察組比4周后觀察組TGF-β1的陽(yáng)性表達(dá)無(wú)明顯變化,差異沒(méi)有統(tǒng)計(jì)學(xué)意義。(P=0.17、P=0.14,P0.05)結(jié)論:1、DCN能夠與膠原纖維高度親和并以此來(lái)調(diào)節(jié)其形成,使其在組織中的表達(dá)受到干擾,穩(wěn)定性變差,進(jìn)而改變其裝配和結(jié)構(gòu),從而抑制瘢痕增生。2、TGF-β1是介導(dǎo)纖維增生性疾病的關(guān)鍵因子,DCN能夠通過(guò)結(jié)合TGF-β1,并且滅活TGF-β1的生物活性,來(lái)抑制瘢痕形成。瘢痕形成的早期纖維化程度比較輕,早期注射效果比較好,而且DCN降解速度適當(dāng),是良好的防治瘢痕的材料。
[Abstract]:Objective: to construct the vocal cord injury model of New Zealand rabbits, and to analyze the pathological changes of vocal cord and the expression of transforming growth factor-尾 1(Transforming factor- 尾 1 (TGF- 尾 1). To observe whether DCN can inhibit vocal cord scar proliferation and to explore the mechanism of DCN inhibiting scar hyperplasia. Methods: 25 New Zealand rabbits were selected and 20 rabbits were randomly selected to make the model of bilateral vocal cord acute injury. The anterior and middle tissues of bilateral vocal cord were clamped by larynx clamp. Ten New Zealand rabbits were immediately injected with 100 渭 g / L core proteoglycan around the injured site of the right vocal cord. The left vocal cord injury site was used as the control vocal cord group A, the other 10 rats were injected with 100 渭 g / L core proteoglycan around the right vocal cord injury site one month after the vocal cord injury, and the other 10 rats were injected with 100 渭 g / L core proteoglycan around the right vocal cord injury site. The injured sites of left vocal cord were used as control vocal cord group B, and the remaining 5 New Zealand rabbits as control group C, group A and group B were randomly selected to harvest vocal cord tissue 4 weeks and 12 weeks after injection of core proteoglycan. The vocal cord tissues harvested from three groups of New Zealand rabbits were stained with HE and immunohistochemistry. The pathological changes of vocal cords and the expression of TGF- 尾 1 were analyzed, and the values of each group were compared and statistically analyzed. Results the vocal cord tissue of New Zealand rabbits was damaged by cyclidine incision, and the animal model of vocal cord injury was successfully constructed. In order to study whether exogenous injection of DCN can inhibit vocal cord scar proliferation, the results of HE staining showed that the undamaged vocal cord tissue in New Zealand rabbits was obviously stratified in order of epithelium, lamina propria and muscularis. The lamina propria is mainly loose connective tissue, and the arrangement of collagen fibers is regular. In the vocal cord injury group, the fibrous tissue of the lamina propria of vocal cord was obviously increased, the collagen fiber was dense, and the arrangement was very messy. The staining of the lamina propria was significantly deeper than that of the non-injuried vocal cord. The fibrous tissue of the lamina propria was increased in the group of DCN injection than that in the non-injured vocal cord. But the arrangement of collagen fibers was regular, the staining was lighter than that of vocal cord injury group, and the positive expression of TGF- 尾 1 was higher in two groups than that in C group, and the expression of TGF- 尾 1 in two groups was higher than that in C group, and the expression of TGF- 尾 1 in group B was higher than that in group C. The positive expression of TGF- 尾 1 in the right vocal cord was significantly lower than that in the left vocal cord, and the difference was statistically significant. The positive expression of TGF- 尾 1 in the right vocal cord group was significantly lower than that in the B group, and the positive expression of TGF- 尾 1 in the right vocal cord group was significantly lower than that in the left vocal cord group. The difference was statistically significant. The positive expression of TGF- 尾 1 in the observation group after 12 weeks was not significantly different from that in the observation group after 4 weeks. The difference was not statistically significant (P < 0. 17, P < 0. 14, P 0. 05). Conclusion: 1. The expression of TGF- 尾 _ 1 in tissues is disturbed, its stability is deteriorated, and its assembly and structure are changed, thus inhibiting scar proliferation. TGF- 尾 _ 1 is a key factor in mediating fibrous hyperplastic disease. DCN can inhibit the biological activity of TGF- 尾 _ 1 by binding to TGF- 尾 _ 1, and inactivating the bioactivity of TGF- 尾 _ 1. To inhibit scar formation. The degree of early fibrosis of scar formation is relatively light, the effect of early injection is better, and the DCN degradation rate is appropriate, so it is a good material for the prevention and treatment of scar.
【學(xué)位授予單位】：山東中醫(yī)藥大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R767.4

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相關(guān)期刊論文 前10條

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本文編號(hào)：1796084