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目的通过研究颈动脉硬化患者人类巨细胞病毒(HCMV)感染状态与脂蛋白a(Lp(a))、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)及ApoB/ApoA1比值的关系,探讨HCMV致动脉硬化的机制。方法利用实时荧光定量PCR技术检测研究对象外周血白细胞中HCMV DNA拷贝数,并利用ELISA技术检测血清中HCMV IgM,同时利用生化分析技术检测Lp(a)、ApoA1、ApoB含量并计算ApoB/ApoA1比值。结果在颈动脉硬化阳性组中,HCMV阳性率为54.7%(35/64),对照组HCMV阳性率为25.0%(5/20),差异有统计学意义(P<0.05);颈动脉硬化阳性组中的Lp(a)、ApoB及ApoB/ApoA1比值均显著高于颈动脉硬化阴性组(0.46±0.31 vs 0.30±0.24,0.77±0.22 vs 0.66±0.18,0.62±0.21 vs 0.51±0.17,P均<0.05),颈动脉硬化阳性组中的ApoA1明显低于颈动脉硬化阴性组(1.35±0.42 vs 1.58±0.41,P<0.05)。在颈动脉硬化阴性组中,HCMV阳性者及HCMV阴性者其ApoA1及ApoB含量差异无统计学意义(1.56±0.44 vs 1.66±0.34,0.67±0.21 vs 0.64±0.10,P均>0.05)。在颈动脉硬化阳性组中,HCMV阳性者血清ApoA1含量明显低于HCMV阴性者(1.27±0.33 vs 1.46±0.34,P<0.05),而ApoB在HCMV阳性者及阴性者中差异无统计学意义(0.78±0.19 vs 0.76±0.15,P>0.05);不论颈动脉硬化阳性组还是对照组,HCMV阳性者的Lp(a)及ApoB/ApoA1比值均显著高于HCMV阴性者(0.59±0.20 vs 0.29±0.17,0.67±0.21 vs 0.56±0.17,0.54±0.36 vs 0.23±0.12,0.58±0.16 vs 0.40±0.14,P均<0.05)。结论 HCMV感染可能通过改变宿主脂类代谢引起或促进动脉硬化的发病过程。
Objective To investigate the relationship between the infection status of human cytomegalovirus (HCMV) and the ratio of lipoprotein a (ApoA1), apolipoprotein B (ApoB) and ApoB / ApoA1 in patients with carotid atherosclerosis, To investigate the mechanism of atherosclerosis in HCMV. Methods HCMV DNA copy number in peripheral blood leukocytes was detected by real-time fluorescence quantitative PCR. HCMV IgM in serum was detected by ELISA. Meanwhile, the contents of Lp (a), ApoA1 and ApoB were detected by biochemical analysis and the ratio of ApoB / ApoA1 . Results The positive rate of HCMV in the carotid atherosclerosis group was 54.7% (35/64), while the positive rate of HCMV in the control group was 25.0% (5/20), the difference was statistically significant (P <0.05); the positive carotid atherosclerosis The ratios of Lp (a), ApoB and ApoB / ApoA1 in the group were significantly higher than those in the carotid atherosclerosis group (0.46 ± 0.31 vs 0.30 ± 0.24, 0.77 ± 0.22 vs 0.66 ± 0.18, 0.62 ± 0.21 vs 0.51 ± 0.17, P <0.05). The ApoA1 in carotid atherosclerosis group was significantly lower than that in carotid atherosclerosis group (1.35 ± 0.42 vs 1.58 ± 0.41, P <0.05). There were no significant differences in ApoA1 and ApoB levels between HCMV positive and HCMV negative patients in carotid atherosclerosis negative (1.56 ± 0.44 vs 1.66 ± 0.34, 0.67 ± 0.21 vs 0.64 ± 0.10, P> 0.05). In carotid atherosclerosis positive group, serum ApoA1 level in HCMV positive patients was significantly lower than that in HCMV negative patients (1.27 ± 0.33 vs 1.46 ± 0.34, P <0.05), while there was no significant difference in ApoB between HCMV positive patients and negative patients ( 0.78 ± 0.19 vs 0.76 ± 0.15, P> 0.05). The ratios of Lp (a) and ApoB / ApoA1 in HCMV positive patients were significantly higher than those in HCMV negative patients (0.59 ± 0.20 vs 0.29 ± 0.17,0.67 ± 0.21 vs 0.56 ± 0.17,0.54 ± 0.36 vs 0.23 ± 0.12,0.58 ± 0.16 vs 0.40 ± 0.14, all P <0.05). Conclusion HCMV infection may cause or promote the pathogenesis of atherosclerosis by changing host lipid metabolism.