【摘要】 目的:评价口内长期感染牙龈卟啉单胞菌（Pg）对载脂蛋白基因敲除小鼠(Apo E^-/-)脂代谢紊乱的影响。方法:取16只SPF级Apo E^-/-雄性小鼠并随机分为两组（n=8）,Aop E^-/--Pg组使用109/m L Pg 33277进行口内涂菌,持续9周,共45次;Aop E^-/--Ct组口内涂抹PBS液。血生化法检测血清中总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）的含量;ELISA法测定小鼠血清Pg特异性Ig G抗体、白细胞介素-6（IL-6）、单核细胞趋化因子-1（MCP-1）以及氧化低密度脂蛋白（ox-LDL）的表达水平;比较两组主动脉粥样硬化（AS）斑块的面积及肝脏病理变化;RT-PCR检测主动脉CD36、ATP结合盒转运子A1（ABCA1）、ATP结合盒转运子G1（ABCG1）的mRNA的表达水平。结果:与Aop E^-/--Ct组相比,Aop E^-/--Pg组血清中Pg特异性IgG抗体明显升高;IL-6、MCP-1表达增加;TC、TG、LDL、ox LDL含量增加,HDL下降;主动脉AS斑块的面积、肝脏脂肪空泡均显著增加;CD36 mRNA表达水平升高,ABCA1、ABCG1mRNA表达水平则无明显变化。结论:口内长期感染Pg可加重Apo E^-/-小鼠脂代谢紊乱,促进AS斑块的进展,而此过程主要由CD36介导。更多还原

【Abstract】 AIM: To assess the effects of long- term oral inoculation with Porphyromonas gingivalis（ Pg） on the lipid metablosim disorder in apolipoprotein E- knocked out( Apo E^-/-) mice. METHODS: 16 Specified Pathogen Free male Apo E^-/-mice were randomly divided into 2 groups. The mice in Aop E^-/-- Pg group were inoculated orally with 109/ m L Pg 33277 for 9 weeks,while those in Aop E^-/-- Ct group were treated with PBS. Blood biochemistry method was used to test the level of TC,TG,HDL,LDL in the serum. ELISA was used to test the level of specific Ig G antibody of Pg,IL- 6,MCP- 1 and ox- LDL in the serum. Red oil"O"stain were used to observe the plague area and in the aorta root. HE staining was used to observe the histopathological changes in liver. Real Time quantitative- PCR was used to monitor the CD36,ABCA1,ABCG1 expression in the aorta. REAULTS: After 9- week inoculation with Pg,the level of specific Pg Ig G antibody,IL- 6,MCP- 1,TC,TG,LDL and ox- LDL was significantly increased and HDL was significantly reduced. The plague area in aorta was bigger and the vacuolar degeneration of liver was more serious. The transcription of CD36 was significantly increased,while the transcription of ABCA1 and ABCG1 had no significant difference. CONLUSION: Long- term oral inoculation with Pg can aggravate the lipid metabolism disorder and accelerate the progression of atherosclerosis in Apo E^-/-mice,which was mediated by CD36.更多还原