Analysis of Correlation Between Coronary Heart Disease and Genetic Polymorphism Detected by Gold Magnetic Nanoparticles Chromatography

被引:0
作者
Cao, Hai-Tao [1 ]
Deng, Cong-ying [2 ]
Yan, Xin-min [3 ]
Lin, Zhi-juan [4 ]
机构
[1] Wenzhou Med Univ, Wenling Peoples Hosp 1, Dept Cardiovasc Med, Wenling 317500, Zhejiang, Peoples R China
[2] Sun Yat Sen Univ, Zhongshan Peoples Hosp, Ultrasound Imaging Dept, Zhongshan 528400, Guangdong, Peoples R China
[3] Nanjing Med Univ, Affiliated Hosp 2, Cent Lab, 68 Gehu Middle Rd, Changzhou 213000, Jiangsu, Peoples R China
[4] Wenzhou Med Univ, Wenling Peoples Hosp 1, Dept Neurol, Wenling 317500, Zhejiang, Peoples R China
关键词
GMNPs; Chromatography; Gene polymorphism; CHD; Glu504Lys; ALDH2; ALDH2 GLU504LYS POLYMORPHISM; ARTERY-DISEASE; MYOCARDIAL-INFARCTION; EAST ASIANS; RISK; SUSCEPTIBILITY; ASSOCIATION; CONTRIBUTES;
D O I
10.1007/s12265-023-10439-w
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It aimed to explore the correlation of Glu504Lys locus mutation of aldehyde dehydrogenase-2 (ALDH2) with coronary heart disease (CHD) based on gold magnetic nanoparticles (GMNPs) chromatography and amplification refractory mutation system-PCR (ARMS-PCR). 120 CHD patients admitted to the cardiovascular Department of Wenling First People's Hospital affiliated to Wenzhou Medical University from December 2020 to December 2021 were selected as Case group and 80 non-CHD patients admitted during the same period were selected as Ctrl group. The venous blood and indexes of Total Cholesterol (TC), Triglyceride (TG), Low Density Lipoprotein Cholesterol (LDL-C), High Density Lipoprotein Cholesterol (HDL-C), and Fasting Blood Glucose (FBS) were collected. The ARMS-PCR GMNPs chromatography based on ARMS-PCR and immunochromatography assay was adopted to detect gene polymorphism of ALDH2. Correlation between ALDH2 gene polymorphism and risk factors of CHD was analyzed via logistic regression. In contrast to Ctrl group, the genotypes of GG, GA, and AA in Case group were evidently different (P < 0.05), and the frequency of A allelic gene was obviously increased (P < 0.05). Under the dominant model, frequency of GA + AA genotype in Case group was remarkably higher in contrast to Ctrl group (P < 0.05). Under the recessive model, there was no obvious difference in genotype frequency between two groups. In contrast to Ctrl group, TC, LDL-C, and FBS in Case group were notably increased (P < 0.05), while HDL-C was notably decreased (P < 0.05). The distribution frequency of abnormal LDL-C, HDL-C, and FBS in Case group was notably higher in contrast to Ctrl group (P < 0.05). LDL-C and FBS had no obvious effect on the genotypes and frequency distribution of alleles in CHD patients. However, the frequency distribution of genotypes of GA and AA and A allelic gene in patients with abnormal HDL-C was notably lower in contrast to those with normal HDL-C (P < 0.05). Logistic regression analysis showed that abnormal HDC-C with A allelic gene were independent risk factors for CHD (P = 0.001, OR = 1.934). The gene polymorphism of Glu504Lys locus of ALDH2 was closely related to the pathogenesis of CHD, A allelic gene may be a susceptibility gene for CHD, and patients with abnormal HDC-C and carried A allelic gene had relatively higher incidence of CHD.
引用
收藏
页码:467 / 475
页数:9
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