林树楷
,陈明磊
,高唯一
,林康.海南地区人群动脉硬化性脑梗死与PCK1启动子-232
基因多态性的相关性研究[J].神经损伤功能重建,2019,14(3):113-115 |
海南地区人群动脉硬化性脑梗死与PCK1启动子-232
基因多态性的相关性研究 |
Relationship between Atherosclerotic Cerebral Infarction and Polymorphism of Phosphoenol⁃pyruvate Carboxykinase Gene Promoter-232 in Hainan Population |
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DOI: |
中文关键词: 脑梗死 PCK1 启动子 多态性 |
英文关键词: cerebral infarction PCK1 promoter polymorphism |
基金项目: |
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中文摘要: |
目的:探讨海南地区人群动脉硬化性脑梗死与磷酸烯醇式丙酮酸羧激酶基因(PCK1)启动子-232基因
多态性的关系。方法:选取动脉硬化性脑梗死患者160例为观察组,另选取同期在我院行健康体检的成年人
160例为对照组,采用聚合酶链反应-限制性片段长度多态性方法检测PCK1启动子-232基因多态性,采用超
声多普勒技术检查颈总动脉内膜中层厚度和颈动脉斑块情况,并监测血糖和血脂情况。结果:观察组中GC
基因型和GG基因型患者的餐后2 h血糖和LDL高于CC基因型(F=12.811,54.169,均P<0.001)。与对照组
相比,观察组中GC和GG基因型频率及G等位基因频率明显较高(χ
2
=13.341、10.807,均P=0.001)。在易损
斑块中,观察组 GC 基因型和 GG 基因型及 G 等位基因的分布明显大于非易损斑块(χ2
=5.186、7.276,P=
0.023、0.007)。2 组不同基因型之间两侧颈总动脉内膜中层厚度比较差异无统计学意义(F=0.742、0.485、
1.139、0.727,P=0.478、0.617、0.325、0.487)。结论:PCK1启动子-232基因多态性与海南地区人群动脉硬化性
脑梗死的发生情况有一定相关性,其中以G等位基因较为突出。 |
英文摘要: |
To explore the relationship between atherosclerotic cerebral infarction and polymorphism of the phosphoenolpyruvate carboxykinase gene (PCK1) promoter-232 in the Hainan population. Meth⁃
ods: We recruited 160 patients with atherosclerotic cerebral infarction as the observation group and another 160
healthy adults who received check-ups during the same time as the control group. PCK1 promoter-232 gene polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP);
the carotid intima-media thickness and carotid artery plaque (CAP) were detected by carotid doppler ultrasonography. The blood glucose and plasma lipids were measured. Results: The 2 h postprandial blood glucose and
LDL cholesterol levels of the GC and GG genotypes in the observation group were higher than those of the CC
genotype (F=12.811, 54.169, both P<0.001). Compared with that of the control group, the frequencies of GC and
GG genotypes and the G allele in the observation group were significantly higher ( χ 2
=13.341, 10.807, all P=
0.001). With vulnerable plaques, the distribution of GC and GG genotypes and the G allele in the observation
group were significantly larger than that with non-vulnerable plaques (χ
2
=5.186, 7.276, P=0.023, 0.007). The carotid intima-media thickness of the left and right carotid artery of different genotypes in the two groups were
compared and showed no statistical difference (F=0.742, 0.485, 1.139, 0.727, P=0.478, 0.617, 0.325, 0.487).
Conclusion: There is a certain connection between PCK1 promoter-232 gene polymorphism and the occurrence
of atherosclerotic cerebral infarction in the population of Hainan, and the role of G allele is more prominent |
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