肺炎衣原体感染增强C57BL/6J小鼠氧化应激加速动脉粥样硬化发展

目的研究肺炎衣原体感染对C57BL/6J小鼠氧化应激及动脉粥样硬化形成的影响。方法48只C57BL/6J小鼠分为感染高脂组、高脂组、感染组和对照组,每组12只,喂养40周,作血清抗CP抗体和血脂水平检测,取主动脉根部标本分析动脉粥样硬化斑块面积,主动脉弓部标本检测超氧阴离子的产生。结果所有接种CP的小鼠,抗CP抗体IgG滴度均大于1∶128,未接种CP者抗CP抗体阴性,感染高脂组和高脂组小鼠血清总胆固醇、低密度脂蛋白水平明显高于对照组,感染高脂组、高脂组和感染组超氧阴离子的产生明显高于对照组(1974.25±650.49)、(701.00±105.16)、(455.62±77.54)counts·mg-1·min-1比(142.25±31.82)counts·mg-1·min-1,P<0.001],氧化荧光染料定位分析发现感染高脂组、高脂组和感染组小鼠主动脉超氧阴离子产生明显增多,且感染高脂组小鼠平均粥样硬化斑块面积大于高脂组(135249±43748)μm2比(96378±30945)μm2,P<0.05]。结论肺炎衣原体感染可加速高脂饮食C57BL/6J小鼠的主动脉粥样硬化发展,并引起C57BL/6J小鼠主动脉超氧阴离子产生增多,提示活性氧产生增多、氧化应激增强可能是肺炎衣原体感染加速动脉粥样硬化发展的机制之一。

Infection with chlamydia pneumoniae increases oxidative stress and accelerates the development of atherosclerosis in C57BL/6J mice

OBJECTIVE: To evaluate the effects of Chlamydia pneumoniae infection on oxidative stress and the development of atherosclerosis in C57BL/6J mice. METHODS: Forty-eight C57BL/6J mice were divided into 4 groups including infection of CP and cholesterol diet, cholesterol diet, infection of CP and control. Atherosclerotic lesions were measured in the aortic root at 40 weeks after the primary infection. Production of superoxide was measured by lucigenin-enhanced chemiluminescence response and evaluated in situ with laser scanning confocal microscope. RESULTS: Infected mice fed with an atherogenic diet developed significantly larger lesion areas compared with the single atherogenic diet mice (135 249 +/- 43 748 microm2 vs. 96 378 +/- 30 945 microm2, P < 0.05). Superoxide generation was higher in aortic arches of the infected mice or atherogenic diet mice compared with the control mice (1974.25 +/- 650.49, 701.00 +/- 105.16, 455.62 +/- 77.54 counts.mg(-1).min(-1) vs. 142.25 +/- 31.82 counts.mg(-1).min(-1), respectively, P < 0.001). CONCLUSION: Chlamydia pneumoniae infection accelerates atherosclerotic lesion development in diet-induced hypercholesterolemic mice. Generation of reactive oxygen species may contribute to atherosclerotic development by Chlamydia pneumoniae infection.