本文關(guān)鍵詞：肺炎衣原體致血管動脈硬化發(fā)生機制的實驗研究　出處：《吉林大學》2006年博士論文　論文類型：學位論文

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

【摘要】：本實驗通過體內(nèi)外病理模型探討了肺炎衣原體感染在動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)皮細胞,用肺炎衣原體(CWL-029)感染血管內(nèi)皮細胞,應用RT-PCR的方法檢測肺炎衣原體對血管內(nèi)皮細胞單核細胞趨化蛋白-1(MCP-1)和白介素-8(IL-8)mRNA表達的影響,進一步應用Western Blot檢測轉(zhuǎn)錄因子(NF-κ Bp65)蛋白的變化,探索NF-κ Bp65在肺炎衣原體致動脈粥樣硬化中的作用及其調(diào)控機制。同時建立C57BL/6J小鼠肺炎衣原體感染動物模型,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)皮細胞,并發(fā)現(xiàn)細胞內(nèi)MCP-1、IL-8 mRNA表達增強,且有時相性變化。IL-8mRNA表達8小時達到高峰,MCP-1 mRNA表達12小時達到高峰。肺炎衣原體感染血管內(nèi)皮細胞,使其細胞核內(nèi)NF-κ Bp65蛋白表達增強,在感染后0.5小時開始增加,1小時達峰值,表明轉(zhuǎn)錄因子NF-κ Bp65明顯的核移位,說明肺炎衣原體激活了血管內(nèi)皮細胞NF-κ B信號傳導通路,通過NF-κ B介導MCP-1、IL-8等炎癥介子的過度表達而在動脈粥樣硬化的發(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)同高脂血癥誘導和/或促進動脈粥樣硬化的形成。大環(huán)內(nèi)脂類藥物通過早期治療預防或延期治療能夠減輕肺炎衣原體感染所致動脈粥樣硬化的形成,肺炎衣原體感染是動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.
【學位授予單位】：吉林大學
【學位級別】：博士
【學位授予年份】：2006
【分類號】：R374

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