蟲草菌粉對兔矽肺纖維化早期干預(yù)作用的研究
發(fā)布時間:2018-03-14 10:29
本文選題:矽肺 切入點:蟲草菌粉 出處:《南昌大學(xué)》2013年碩士論文 論文類型:學(xué)位論文
【摘要】:背景:當(dāng)前,從接觸粉塵的人數(shù)、新發(fā)矽肺人數(shù)及現(xiàn)患病人數(shù)來講,中國是受矽肺危害最嚴(yán)重的國家。矽肺發(fā)病機(jī)制至今尚未不清楚,學(xué)者們曾提出過諸多假說,盡管各個學(xué)說都有其合理之處,但都難以確切地描述其發(fā)病機(jī)制。近年來,TGF-β被大多數(shù)學(xué)者公認(rèn)為是肺纖維化形成與發(fā)展的關(guān)鍵性細(xì)胞因子。在多種纖維增生性疾病中,TGF-β表現(xiàn)出共同促纖維化作用,其中TGF-β1為TGF-β家族中最重要的致纖維化的亞型,而Smad7蛋白是一種新發(fā)現(xiàn)的蛋白,是TGF-β-Smads信號通路的下游蛋白,,其異常表達(dá)在肺纖維化發(fā)生發(fā)展中起關(guān)鍵作用。已有很多研究表明TGF-β1和Smad7在肺纖維化發(fā)病過程中發(fā)揮重要的作用,本實驗通過測定上述兩種因子在各組兔肺組織中的表達(dá),探討其在矽肺纖維化發(fā)病過程中的可能機(jī)制。 目的:成功復(fù)制兔矽肺模型,探討蟲草菌粉對兔矽肺纖維化形成過程中的干預(yù)作用。 方法:選取30只健康雄性大耳白兔,隨機(jī)均分為三組,即:1、空白對照組(BP),2、矽肺對照組(CP),3、實驗干預(yù)組(EP),CP、EP組氣管內(nèi)注入二氧化硅粉塵懸液,BP組氣管內(nèi)注入相同體積的生理鹽水。兔染矽塵30d后處死,計算肺重系數(shù),右肺組織行HE染色,運用加堿水解法測定免肺組織的羥脯氨酸含量,實時熒光定量PCR法測免肺組織TGF-β1及Smad7的mRNA表達(dá)水平。 結(jié)果:3組兔肺組織HE染色示:BP組正常肺組織,CP、EP組兔肺組織明顯纖維化并有矽肺結(jié)節(jié)形成,顯示矽肺兔模型造模成功。在三組兔肺組織中,肺重系數(shù)和羥脯氨酸的含量存在顯著差異(P0.05)。 EP組與BP組間比較:免肺組織TGF-β1表達(dá)水平升高及Smad7表達(dá)水平下降(P0.02);EP組與CP組比較:免肺組織TGF-β1表達(dá)水平下降及Smad7表達(dá)水平升高P0.05)。 結(jié)論:蟲草菌粉在兔矽肺纖維化形成的過程具有一定的影響,可能是通過減少TGF-β1mRNA表達(dá),依賴于TGF-β-Smads信號通路來上調(diào)smad7mRNA,從而對兔矽肺纖維化的形成有一定抑制作用。
[Abstract]:Background: in terms of the number of people exposed to dust, the number of newly developed silicosis and the number of people suffering from silicosis, China is the most seriously affected by silicosis. The pathogenesis of silicosis is not yet clear, and scholars have put forward many hypotheses. Although each doctrine has its own reasonableness, In recent years, TGF- 尾 has been recognized by most scholars as the key cytokine in the formation and development of pulmonary fibrosis. TGF- 尾 plays a common role in promoting fibrosis in various fibroproliferative diseases. TGF- 尾 1 is the most important fibrogenic subtype of TGF- 尾 family, and Smad7 protein is a newly discovered protein, which is downstream of TGF- 尾 -Smads signaling pathway. Many studies have shown that TGF- 尾 1 and Smad7 play an important role in the pathogenesis of pulmonary fibrosis. To explore its possible mechanism in the pathogenesis of silicosis fibrosis. Aim: to establish rabbit silicosis model successfully and to investigate the effect of cordyceps powder on the formation of silicosis in rabbits. Methods: thirty healthy male rabbits were randomly divided into three groups. The rats in the intervention group were injected with the same volume of normal saline into the trachea of the EPX CPEP group and the BP group with silica dust suspension. After 30 days of exposure to silica dust, the rabbits were killed, the lung weight coefficient was calculated, and the right lung tissue was stained with HE. The content of hydroxyproline in lung tissues was determined by alkaline hydrolysis, and the mRNA expression of TGF- 尾 1 and Smad7 in lung tissues was measured by real-time fluorescence quantitative PCR. Results the lung tissues of the three groups showed obvious fibrosis and silicosis nodule formation in the normal lung tissue of the control group and the CPEP group, indicating that the silicosis rabbit model was successfully established, and in the lung tissue of the three groups, the lung tissue of the control group and the control group were observed. There was significant difference in lung weight coefficient and hydroxyproline content between EP group and BP group. The expression level of TGF- 尾 1 and Smad7 decreased in EP group compared with CP group. Compared with CP group, the expression level of TGF- 尾 1 and Smad7 increased P0.05in EP group. Conclusion: Cordyceps powder has a certain effect on the formation of silicosis in rabbits, which may be due to the decrease of TGF- 尾 1 mRNA expression and the up-regulation of smad7mRNAs by TGF- 尾 -Smads signaling pathway, which may inhibit the formation of silicosis in rabbits.
【學(xué)位授予單位】:南昌大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2013
【分類號】:R135.2
【引證文獻(xiàn)】
相關(guān)碩士學(xué)位論文 前1條
1 黃彥銘;補(bǔ)陽還五湯對肺纖維化大鼠肺泡灌洗液中HMGB1,IL-8,α-SMA水平影響的實驗研究[D];成都中醫(yī)藥大學(xué);2015年
本文編號:1610811
本文鏈接:http://sikaile.net/yixuelunwen/huxijib/1610811.html
最近更新
教材專著