IL-6、TGF-β1在尿道損傷黏膜中的表達(dá)及作用
本文關(guān)鍵詞: 尿道損傷 IL-6 TGF-β1 纖維化 炎癥 出處:《河北醫(yī)科大學(xué)》2017年碩士論文 論文類型:學(xué)位論文
【摘要】:目的:探討IL-6、TGF-β1在尿道損傷黏膜中的表達(dá)及作用。方法:1通過用導(dǎo)絲對小鼠尿道組織損傷建立尿道損傷模型。對正常尿道小鼠和尿道損傷小鼠的尿道組織進(jìn)行蘇木精-伊紅染色(HE)觀察和評價尿道黏膜的形態(tài)學(xué)改變。2實時定量PCR(q RT-PCR)檢測正常尿道小鼠和尿道損傷小鼠的尿道組織IL-6、TGF-β1 mRNA的表達(dá)。3 IL-6、TGF-β1基因熒光探針聯(lián)合MAC2原位雜交定位基因的表達(dá)。結(jié)果:1尿道損傷小鼠尿道組織增生明顯,黏膜層厚度顯著增加,管腔狹窄率增高。HE染色結(jié)果顯示,與正常尿道組織相比,尿道損傷小鼠尿道組織增生顯著,黏膜層厚度(303.2±21.4μm)顯著增加(P0.05),尿道管腔狹窄率達(dá)90.67%,顯著大于正常尿道組織的41.56%(P0.01)。2尿道損傷組織IL-6、TGF-β1 mRNA表達(dá)量顯著高于正常尿道組織。實時定量PCR結(jié)果顯示,正常尿道組織的IL-6、TGF-β1 mRNA表達(dá)增加僅為0.9和1.2倍,而尿道損傷組織表達(dá)增加各為2.5和4.3倍,表達(dá)顯著增加。3尿道損傷組織中的炎癥浸潤增加,主要表現(xiàn)為炎性因子IL-6、TGF-β1表達(dá)增加及巨噬細(xì)胞浸潤加劇。IL-6、TGF-β1基因熒光探針結(jié)合MAC2免疫染色的原位雜交結(jié)果顯示,IL-6探針-MAC2、TGF-β1探針-MAC2陽性率在尿道損傷組織中顯著高于正常尿道組織。結(jié)論:IL-6和TGF-β1在尿道損傷組織中高表達(dá)水平,促使炎性細(xì)胞的激活和浸潤,兩者相互作用,導(dǎo)致尿道黏膜組織慢性增生、纖維化,促進(jìn)尿道狹窄的形成和發(fā)展。
[Abstract]:Objective: to investigate the expression and role of IL-6 TGF- 尾 1 in urethral mucous membrane injury. Methods: the urethral injury model of mice was established by using the guide wire. The urethral tissue of normal urethral mice and urethral injury mice were treated with hematoxylum thuringiensis. Observation and evaluation of morphologic changes of urethral mucosa by sperm-eosin staining. 2 Real-time quantitative PCR(q RT-PCR) to detect the expression of IL-6TGF- 尾 1 mRNA in urethral tissues of normal and injured urethra mice. The expression of IL-6 TGF- 尾 1 gene fluorescence probe combined with MAC2 in situ hybridization assay was used to detect the expression of IL-6 TGF- 尾 1 gene in urethral tissue of mice with urethral injury. Results the urethral tissue proliferation in mice with urethral injury was obvious. Compared with normal urethral tissue, urethral tissue proliferation in mice with urethral injury was significantly higher than that in normal urethral tissue. The mucosal thickness (303.2 鹵21.4 渭 m) significantly increased the expression of IL-6 TGF- 尾 1 mRNA in urethral tissue, and the urethral stricture rate was 90.67, which was significantly higher than that in normal urethral tissue. The expression of IL-6 TGF- 尾 1 mRNA in urethral injury tissue was significantly higher than that in normal urethral tissue. The expression of IL-6 TGF- 尾 1 mRNA in normal urethra was only 0.9-fold and 1.2-fold higher than that in urethral injury, and the expression of IL-6TGF- 尾 _ 1 in urethral injury was increased by 2.5 and 4.3 times, respectively. The expression of IL-6 TGF- 尾 _ 1 increased significantly in urethral injury tissue. The results of in situ hybridization with fluorescence probe of TGF- 尾 1 gene and MAC2 immunostaining showed that the positive rate of IL-6 probe -MAC2TGF- 尾 1 probe in urethral injury tissue was significantly higher than that of normal tissue. Conclusions the expression of TGF- 尾 1 and IL-6 in urethral injury tissue is higher than that in urethral injury tissue. Promote inflammatory cell activation and infiltration, the interaction between the two leads to chronic hyperplasia of urethral mucosal tissue, fibrosis, promote the formation and development of urethral stricture.
【學(xué)位授予單位】:河北醫(yī)科大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2017
【分類號】:R695
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