本文選題：異常黑膽質(zhì)成熟劑　切入點：增生性瘢痕　出處：《新疆醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:研究不同濃度的維藥異常黑膽質(zhì)成熟劑ASMq對體外培養(yǎng)增生性瘢痕成纖維細(xì)胞遷移率及增殖的影響及對相關(guān)蛋白表達(dá)的影響,進而從不同層面探索對增生性瘢痕生長的抑制作用。方法:采用酶消法體外培養(yǎng)人增生性瘢痕成纖維細(xì)胞,將其分為6組:正常皮膚組:空白對照組:實驗組3組(分別加入不同濃度ASMq0.2mg/ml,0.35 mg/ml,0.5mg/ml)及陽性組(加入5-氟尿嘧啶0.2mg/ml),對各組細(xì)胞進行相應(yīng)藥物干預(yù),采用細(xì)胞遷移實驗,CCK-8、Western blot實驗檢查應(yīng)用維藥異常黑膽質(zhì)成熟劑后細(xì)胞遷移率、增殖作用與轉(zhuǎn)化生長因子β/Smad信號通路的改變。結(jié)果:在同一時間,與正常皮膚組比較,空白對照組增生性瘢痕成纖維遷移率明顯增加(P0.05),與空白對照組比較,隨著ASMq-TF濃度增加,增生性瘢痕成纖維細(xì)胞遷移率逐漸減少(P0.05)。ASMq下調(diào)了TGF-β1誘導(dǎo)的成纖維細(xì)胞CollagenⅠ及CollagenⅢ的表達(dá)(P0.05),同時,ASMq明顯增加了被TGF-β1抑制的Smad7 mRNA和Smad7的表達(dá)(P0.05)。結(jié)論:研究結(jié)果表明隨著ASMq濃度的增加,增生性瘢痕成纖維細(xì)胞遷移率被抑制,且ASMq可通過促進Smad7合成來阻斷增生性瘢痕成纖維細(xì)胞TGF-β/Smad通路信號轉(zhuǎn)導(dǎo),從而降低成纖維細(xì)胞增殖及CollagenⅠ合成。
[Abstract]:Aim: to study the effects of different concentrations of ASMq on the migration and proliferation of hypertrophic scar fibroblasts and the expression of related proteins. Methods: human hypertrophic scar fibroblasts were cultured in vitro by enzyme digestion method. They were divided into 6 groups: normal skin group: blank control group: experimental group 3 (add different concentration ASMQ 0.2 mg / ml 0.35 mg / ml) and positive group (add 5-fluorouracil 0.2 mg / ml 路ml ~ (-1)). The cell migration rate, proliferation and transforming growth factor 尾 -Smad signaling pathway were detected by CCK-8 blot assay. Results: at the same time, compared with normal skin group, the cell migration rate, proliferation and transforming growth factor 尾 -Smad signaling pathway were measured. The migration rate of hypertrophic scar fibroblasts in the blank control group was significantly higher than that in the blank control group, and compared with the control group, with the increase of ASMq-TF concentration, The migration rate of hypertrophic scar fibroblasts decreased gradually (P 0.05). ASMq down-regulated the expression of Collagen 鈪，

本文編號：1584930