【摘要】：目的:本研究在維吾爾醫(yī)學(xué)(維醫(yī))體液論的指導(dǎo)下成功建立異常膽液質(zhì)載體潰瘍性結(jié)腸炎(Ulcerative colitis,UC)病證大鼠模型,檢測異常膽液質(zhì)載體UC病證模型組和正常組大鼠結(jié)腸組織中IL-1α、IL-1β、iNOS、eNOS等四種炎癥相關(guān)因子的hnRNA和mRNA表達(dá)水平的變化及NF-κB對上述四種炎癥相關(guān)因子基因轉(zhuǎn)錄活性的調(diào)控機(jī)制,從而闡述NF-κB在異常膽液質(zhì)載體UC病證發(fā)生、發(fā)展中的作用機(jī)制。方法:根據(jù)維醫(yī)體液論建立異常膽液質(zhì)載體證候模型的基礎(chǔ)上,采用TNBS/乙醇法構(gòu)建異常膽液質(zhì)載體UC病證大鼠模型,將動物分為正常組和異常膽液質(zhì)載體UC病證模型組,應(yīng)用實時熒光定量逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(qRT-PCR)方法檢測兩組大鼠結(jié)腸組織中IL-1α、IL-1β、iNOS、e NOS的hnRNA與mRNA表達(dá)水平,并分析其表達(dá)差異,應(yīng)用染色質(zhì)免疫共沉淀(Chromatin Immunoprecipitation,ChIP)-qPCR方法,檢測NF-κB與候選基因IL-1α、IL-1β、iNOS、eNOS調(diào)控序列的親和力,闡述存在表達(dá)差異的分子機(jī)制。結(jié)果:1)異常膽液質(zhì)載體UC病證模型組大鼠體征、癥狀、結(jié)腸粘膜損傷等均符合異常膽液質(zhì)載體UC病證模型的判定標(biāo)準(zhǔn);2)qRT-PCR結(jié)果顯示,與正常組比較,異常膽液質(zhì)載體UC病證模型組大鼠結(jié)腸組織中IL-1α、IL-1β、iNOS的hnRNA表達(dá)水平均上調(diào),差異有統(tǒng)計學(xué)意義(P0.05),而eNOS的hnRNA表達(dá)水平無統(tǒng)計學(xué)意義(P0.05);與正常組比較,異常膽液質(zhì)載體UC病證模型組大鼠結(jié)腸組織中IL-1α、IL-1β、iNOS、eNOS的mRNA表達(dá)水平均上調(diào),差異有統(tǒng)計學(xué)意義(P0.05);3)ChIP-qPCR結(jié)果顯示,與正常組比較,異常膽液質(zhì)載體UC病證模型組大鼠結(jié)腸組織中NF-κB增強(qiáng)IL-1α、IL-1β、iNOS基因的轉(zhuǎn)錄活性,而對eNOS基因轉(zhuǎn)錄活性的調(diào)控作用不明顯。結(jié)論:1)異常膽液質(zhì)載體UC病證模型組大鼠結(jié)腸組織中出現(xiàn)免疫功能紊亂;2)異常膽液質(zhì)載體UC病證模型組大鼠結(jié)腸組織中NF-κB通過與IL-1α、IL-1β、iNOS等候選基因調(diào)控序列的結(jié)合,增強(qiáng)候選基因的轉(zhuǎn)錄活性,從而促進(jìn)候選基因的表達(dá);3)異常膽液質(zhì)載體UC病證大鼠結(jié)腸組織中炎癥相關(guān)因子表達(dá)水平的調(diào)控除了NF-κB的轉(zhuǎn)錄水平調(diào)控作用外,還可能存在RNA的穩(wěn)定性相關(guān)的轉(zhuǎn)錄后調(diào)控機(jī)制。
[Abstract]:Objective: to establish the rat model of ulcerative colitis (Ulcerative colitis,UC) with abnormal bile fluid carrier under the guidance of Uighur medicine (Uighur medicine) theory of body fluid. Detection of IL-1 偽, IL-1 尾, iNOS, in colonic tissue of rats with abnormal choledochal carrier UC disease model group and normal group The changes of hnRNA and mRNA expression levels of eNOS and other four inflammatory related factors and the regulation mechanism of NF- 魏 B on the transcriptional activity of the above four inflammatory related factors were discussed in order to elucidate the occurrence of NF- 魏 B in abnormal choledochal vector UC disease, and the mechanism of the regulation of NF- 魏 B on the transcription activity of these four inflammatory related factors. Mechanisms of action in development Methods: on the basis of establishing the syndrome model of abnormal choledochal carrier according to the theory of Uygur liquid, the rat model of abnormal choledochal carrier UC syndrome was established by TNBS/ ethanol method. The rats were divided into normal group and abnormal choledochal carrier UC syndrome model group, and the rats were divided into two groups: normal group and abnormal choledochal carrier model group. Real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of IL-1 偽, IL-1 尾, iNOS,e NOS hnRNA and mRNA in colon tissues of two groups of rats, and the difference was analyzed. Chromatin immunoprecipitation (Chromatin Immunoprecipitation,ChIP)-qPCR was used to detect the affinity of NF- kappa B to the regulatory sequences of candidate genes IL-1 偽, IL-1 尾 and iNOS,eNOS, and to elucidate the molecular mechanism of the differential expression. Results: 1) the signs, symptoms and colonic mucosal injury of rats in the model group of abnormal choledochal carrier UC's disease met the criteria of abnormal choledochal carrier UC's disease model; 2) the results of qRT-PCR showed that the expression of IL-1 偽, IL-1 尾 and iNOS hnRNA in colon tissue of rats in abnormal choledochal carrier UC syndrome group were up-regulated compared with the normal group (P0.05), and there was a significant difference between the two groups (P0.05). The expression level of hnRNA in eNOS was not statistically significant (P0.05). Compared with the normal group, the expression levels of IL-1 偽, IL-1 尾 and iNOS,eNOS mRNA in colon tissue of the model group with abnormal choledochal carrier UC disease were up-regulated (P0.05). 3) the results of ChIP-qPCR showed that NF- 魏 B enhanced the transcriptional activity of IL-1 偽, IL-1 尾 and iNOS genes in colon tissue of rats in abnormal bile carrier UC syndrome group, but did not regulate the transcriptional activity of eNOS gene. Conclusion: 1) in the model group of abnormal choledochal carrier UC's disease, there is an immune disorder in the colon tissue of rats. 2) in the model group of abnormal choledochal vector UC syndrome, NF- kappa B combined with IL-1 偽, IL-1 尾, iNOS and other candidate gene regulatory sequences to enhance the transcriptional activity of candidate genes and thus promote the expression of candidate genes. 3) the regulation of inflammation-associated factor expression in colon of rats with abnormal choledochal carrier UC disease may also have the mechanism of RNA stability-related post-transcriptional regulation, in addition to the regulation of NF- 魏 B transcription level.
【學(xué)位授予單位】：新疆醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2016
【分類號】：R29

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