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肺炎衣原体感染对高脂血症小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、P50和c-Fos表达的影响 被引量:1

Effect of Chlamydia Pneumoniae Infection on Expression of Peroxisome Proliferator-Activated Receptor γ,P50 and c-Fos in Aortic Endothelial Cell in Hyperlipidemia Mice.
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摘要 目的探讨肺炎衣原体感染对高脂血症小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、核因子κB和激活蛋白1表达的影响。方法48只C57BL/6J雌性小鼠分成对照组、感染组、高脂组和感染高脂组。14周后,通过间接免疫荧光标记法检测主动脉内皮细胞过氧化体增殖物激活型受体γ、P50(核因子κB亚单位)和c-Fos(激活蛋白1亚单位)表达情况。用苏丹Ⅳ对主动脉窦冰冻切片进行脂染色以检测主动脉窦动脉粥样硬化病灶情况并进行评分。结果主动脉窦动脉粥样硬化病灶评分在对照组和感染组无升高,而在高脂组和感染高脂组显著升高(P<0.01),且感染高脂组和高脂组相比差异有显著性(P<0.01)。和对照组相比,感染组、高脂组和感染高脂组小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、P50和c-Fos的表达是升高的,而在感染组、高脂组和感染高脂组3组之间过氧化体增殖物激活型受体γ、P50和c-Fos的表达差异无显著性。结论在肺炎衣原体感染和高脂血症的早期,小鼠主动脉内皮细胞的炎症通路已经激活。单独肺炎衣原体感染不能引起动脉粥样硬化的形成,但肺炎衣原体感染能加速高脂饮食引起的动脉粥样硬化形成。 Aim To investigate the effect of C.pneumoniae infection on the expression of peroxisome proliferator-activated receptor γ(PPARγ),nuclear factor-κB (NF-κB) and activated protein-1 (AP-1 ) in aortic endothelial cell in hyperhpidemia mice. Methods Forty-eight, 8-week-old female C57BL/6J mice were divided into 4 groups: control group, infected group, atherogenic diet group and infected atherogenic diet group ( each twelve). 14 weeks later, the expression of PPARγ, P50 ( subunit of NF-κB} and c-Fos( subunit of AP-1) was determined by indirect immunofluorescence in the aortic endothelial cell. Slides of aortic sinus were prepared by cryosection, and stained with Sudan Ⅳ for examination of atherosclerotic plaque. The score of atherosclerotic plaque was determined by microscopy. Results The score of atherosclerotic plaque in infected group was not increased, while it was significant higher in atherogenic diet group and infected atherogenic diet group (P〈0.01 ), still the score in infected atherogenic diet group was ldgher than in atherogenic diet group ( P〈0.01). The expression of PPARγ,NF-κB and AP-1 in endothelial cell in aortic sinus was upregulated in infected group, atherogenic diet group and infected atherogenic diet group, in comparison with that in control group (P〈0.05). There was no significant difference among infected group, atherogenic diet group and infected atherogemc diet group. Conclusion The inflammatory process was already initiated in the aortic endothelial cell in C57BL/6J mice at the early stage of Chlanrydia pneumoniae infection and hyperlipidemia. Chlamydia pneumoniae infection alone would not accelerate the process of atherosclerosis. But Chlamydia pneumoniae infection could accelerate the process of atherosclerosis.
出处 《中国动脉硬化杂志》 CAS CSCD 2006年第1期32-36,共5页 Chinese Journal of Arteriosclerosis
基金 广州市科委基金(No:1999-Z-102-02)
关键词 病理学与病理生理学 肺炎衣原体感染是动脉硬化的辅助因子 肺炎衣原体 高脂血症 过氧化体增殖物激活型受体Γ P50 c-Yos Chlamydia Pneumoniae Hypercholesterolemia Peroxisome Proliferator-Acfivated Receptor γ P50 c-Fos Endothehum
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