本文關(guān)鍵詞：肺炎衣原體致血管動(dòng)脈硬化發(fā)生機(jī)制的實(shí)驗(yàn)研究　出處：《吉林大學(xué)》2006年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 肺炎衣原體 動(dòng)脈粥樣硬化 白介素-8 單核細(xì)胞趨化蛋白-1 核轉(zhuǎn)錄因子 動(dòng)物模型

【摘要】：本實(shí)驗(yàn)通過(guò)體內(nèi)外病理模型探討了肺炎衣原體感染在動(dòng)脈粥樣硬化形成和發(fā)展中的作用。體外培養(yǎng)人臍靜脈血管內(nèi)皮細(xì)胞,用肺炎衣原體(CWL-029)感染血管內(nèi)皮細(xì)胞,應(yīng)用RT-PCR的方法檢測(cè)肺炎衣原體對(duì)血管內(nèi)皮細(xì)胞單核細(xì)胞趨化蛋白-1(MCP-1)和白介素-8(IL-8)mRNA表達(dá)的影響,進(jìn)一步應(yīng)用Western Blot檢測(cè)轉(zhuǎn)錄因子(NF-κ Bp65)蛋白的變化,探索NF-κ Bp65在肺炎衣原體致動(dòng)脈粥樣硬化中的作用及其調(diào)控機(jī)制。同時(shí)建立C57BL/6J小鼠肺炎衣原體感染動(dòng)物模型,并觀察了大環(huán)內(nèi)脂類藥物(克拉霉素)的治療效果。結(jié)果表明:肺炎衣原體能夠感染臍靜脈血管內(nèi)皮細(xì)胞,并發(fā)現(xiàn)細(xì)胞內(nèi)MCP-1、IL-8 mRNA表達(dá)增強(qiáng),且有時(shí)相性變化。IL-8mRNA表達(dá)8小時(shí)達(dá)到高峰,MCP-1 mRNA表達(dá)12小時(shí)達(dá)到高峰。肺炎衣原體感染血管內(nèi)皮細(xì)胞,使其細(xì)胞核內(nèi)NF-κ Bp65蛋白表達(dá)增強(qiáng),在感染后0.5小時(shí)開(kāi)始增加,1小時(shí)達(dá)峰值,表明轉(zhuǎn)錄因子NF-κ Bp65明顯的核移位,說(shuō)明肺炎衣原體激活了血管內(nèi)皮細(xì)胞NF-κ B信號(hào)傳導(dǎo)通路,通過(guò)NF-κ B介導(dǎo)MCP-1、IL-8等炎癥介子的過(guò)度表達(dá)而在動(dòng)脈粥樣硬化的發(fā)生發(fā)展中起作用。肺炎衣原體感染加重了高脂血癥小鼠的IL-6和IL-8水平的升高,表明肺炎衣原體感染協(xié)同高脂血癥誘導(dǎo)和/或促進(jìn)動(dòng)脈粥樣硬化的形成。大環(huán)內(nèi)脂類藥物通過(guò)早期治療預(yù)防或延期治療能夠減輕肺炎衣原體感染所致動(dòng)脈粥樣硬化的形成,肺炎衣原體感染是動(dòng)脈粥樣硬化形成和發(fā)展的因素之一。
[Abstract]:In this study, the role of chlamydia pneumoniae infection in the formation and development of atherosclerosis in vitro and in vivo was studied. Human umbilical vein endothelial cells were cultured in vitro. The vascular endothelial cells were infected with chlamydia pneumoniae (CWL-029). The effects of chlamydia pneumoniae on the expression of monocyte chemoattractant protein (MCP-1) and interleukin-8 (IL-8) mRNA in vascular endothelial cells were detected by RT-PCR. Furthermore, Western Blot was used to detect the change of NF- 魏 Bp65) protein. To explore the role of NF- 魏 Bp65 in chlamydia pneumoniae induced atherosclerosis and its regulatory mechanism, and to establish C57BL / 6J mice model of chlamydia pneumoniae infection. The results showed that chlamydia pneumoniae could infect endothelial cells of umbilical vein and found intracellular MCP-1. The expression of IL-8mRNA was enhanced, and sometimes the expression of IL-8 reached its peak at 8 hours after phase change. The expression of MCP-1 mRNA reached its peak at 12 hours. Chlamydia pneumoniae infected vascular endothelial cells (VEC) and increased the expression of NF- 魏 Bp65 protein in the nucleus of chlamydia pneumoniae. The peak value of NF- 魏 Bp65 increased to 1 hour at 0.5 h after infection, indicating that the nuclear translocation of the transcription factor NF- 魏 Bp65 was obvious. These results suggest that chlamydia pneumoniae activates NF- 魏 B signaling pathway in vascular endothelial cells and mediates MCP-1 through NF- 魏 B. The overexpression of inflammatory mesons such as IL-8 plays an important role in the development of atherosclerosis. Chlamydia pneumoniae infection exacerbates the increase of IL-6 and IL-8 levels in hyperlipidemic mice. The results indicate that chlamydia pneumoniae infection combined with hyperlipidemia induces and / or promotes the formation of atherosclerosis. Macrocyclic lipids can reduce atherosclerosis caused by chlamydia pneumoniae infection by early treatment or delayed treatment. The formation of metamorphosis. Chlamydia pneumoniae infection is one of the factors in the formation and development of atherosclerosis.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2006
【分類號(hào)】：R374

【參考文獻(xiàn)】

相關(guān)期刊論文 前5條

1 施毅,康曉明,宋勇,張曉琦,夏錫榮;基因擴(kuò)增法檢測(cè)肺炎衣原體DNA的研究[J];金陵醫(yī)院學(xué)報(bào);1995年02期

2 王衛(wèi)群,袁佶,王岫南,余竹元;家兔的肺炎衣原體感染和動(dòng)脈粥樣硬化模型[J];上海醫(yī)科大學(xué)學(xué)報(bào);2000年04期

3 高昭景,張嬰元,楊帆,范維琥;冠心病患者肺炎衣原體感染的調(diào)查[J];復(fù)旦學(xué)報(bào)(醫(yī)學(xué)版);2003年03期

4 余竹元,項(xiàng)俊慶,李子華;肺炎衣原體對(duì)不同細(xì)胞株的敏感性研究[J];中國(guó)人獸共患病雜志;1999年06期

5 姚詠明,盛志勇;膿毒癥信號(hào)轉(zhuǎn)導(dǎo)機(jī)制的現(xiàn)代認(rèn)識(shí)[J];中國(guó)危重病急救醫(yī)學(xué);2003年01期

，

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