海南籍黎族和汉族急性脑梗死患者C反应蛋白和白细胞介素18的基因多态性研究
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摘要
目的探讨C反应蛋白(CRP)-1059 G/C,白细胞介素18(IL-18)启动子基因-607 C/A和-137 G/C位点的基因多态性与海南黎、汉族人群急性脑梗死的相关性。方法选择汉族脑梗死患者115例为汉族脑梗死组和黎族脑梗死患者52例为黎族脑梗死组,分别与健康的汉族对照组116例和黎族对照组51例对照研究。测定CRP-1059 G/C、IL-18启动子基因-607 C/A和-137 G/C位点基因多态性。结果汉族脑梗死组CRP-1059 G/C位点C等位基因频率与汉族对照组比较,差异有统计学意义(P=0. 044),并且CRP-1059 G/C位点GG+GC基因型频率明显高于汉族对照组,CC基因型明显低于汉族对照组(78. 3%vs 87. 9%),差异有统计学意义(P=0. 049)。黎族脑梗死组CRP-1059 G/C、IL-18-607 C/A及IL-18-137 G/C位点的基因型和等位基因频率与黎族对照组比较,差异无统计学意义(P> 0. 05)。多因素logistic回归分析显示,CRP-1059 GG+GC基因型为汉族脑梗死患者的独立危险因素(P <0. 05)。结论 CRP-1059 GG+GC基因型是海南籍汉族脑梗死患者的独立危险因素。而IL-18-607 C/A、IL-18-137 G/C基因多态性均与海南籍黎、汉族脑梗死患者无关。
Objective To study the relationship of CRP promoter 1059 G/C,IL-18 promotor 607 C/A,IL-18 promotor 137 G/C polymorohisms with acute cerebral infarction( ACI) in Hainan Li and Han patients. Methods One hundred and fifteen Han ACI patients served as a Han ACI group and 52 Li ACI patients served as a Li ACI group with 116 healthy Han subjects served as a Han control group and 51 healthy Li subjects served as a Li control group. Their CRP promoter 1059 G/C,IL-18 promotor 607 C/A,IL-18 promotor 137 G/C polymorohisms were detected. Results No significant difference was found in allelic genotype frequency at CRP-1059 G/C between Han ACI group and Han control group( P = 0.044). The rate of GG + GC genotype frequency at CRP-1059 G/C was significantly higher while that of CC genotype frequency at CRP-1059 G/C was significantly lower in Han ACI group than in Han control group( 78. 3% vs 87. 9%,P = 0. 049). No significant difference was found in genotype and allelic gene requency at CRP-1059 G/C,IL-18-607 C/A and IL-18-137 G/C between Li ACI group and Li control group( P > 0. 05). Multivariate logistic regression analysis showed that CRP-1059 GG + GC genotype was an independent risk factor for ACI in Hainan Han patients( P < 0. 05). Conclusion CRP-1059 GG +GC genotype is an independent risk factor for ACI in Hainan Han patients. IL-18-607 C/A and IL-18-137 G/C gene polymorphisms are not related with ACI in Hainan Han and Li patients.
Objective To study the relationship of CRP promoter 1059 G/C,IL-18 promotor 607 C/A,IL-18 promotor 137 G/C polymorohisms with acute cerebral infarction( ACI) in Hainan Li and Han patients. Methods One hundred and fifteen Han ACI patients served as a Han ACI group and 52 Li ACI patients served as a Li ACI group with 116 healthy Han subjects served as a Han control group and 51 healthy Li subjects served as a Li control group. Their CRP promoter 1059 G/C,IL-18 promotor 607 C/A,IL-18 promotor 137 G/C polymorohisms were detected. Results No significant difference was found in allelic genotype frequency at CRP-1059 G/C between Han ACI group and Han control group( P = 0.044). The rate of GG + GC genotype frequency at CRP-1059 G/C was significantly higher while that of CC genotype frequency at CRP-1059 G/C was significantly lower in Han ACI group than in Han control group( 78. 3% vs 87. 9%,P = 0. 049). No significant difference was found in genotype and allelic gene requency at CRP-1059 G/C,IL-18-607 C/A and IL-18-137 G/C between Li ACI group and Li control group( P > 0. 05). Multivariate logistic regression analysis showed that CRP-1059 GG + GC genotype was an independent risk factor for ACI in Hainan Han patients( P < 0. 05). Conclusion CRP-1059 GG +GC genotype is an independent risk factor for ACI in Hainan Han patients. IL-18-607 C/A and IL-18-137 G/C gene polymorphisms are not related with ACI in Hainan Han and Li patients.
引文
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[11]戴肖力,王占强.白细胞介素18基因启动子区-607 C/A多态性与缺血性卒中的相关性[J].河北医科大学学报,2014,35(6):681-683. DOI:10. 3969/j. issn. 1007-3205. 2014. 06.020.
[12] Liu Y,Geng PL,Yan FQ,et al. C-reactive protein-717A> G and-286C> T> A gene polymorphism and ischemic stroke[J]. Chin Med J(Engl),2015,128(12):1666-1670. DOI:10. 4103/0366-6999. 158371.
[2] Martín A,Domercq M,Matute C. Inflammation in stroke:the role of cholinergic,purinergic and glutamatergic signaling[J]. Ther Adv Neurol Disord,2018,11:1756286418774267. DOI:10.1177/1756286418774267.
[3] Fann DY,Lee SY,Manzanero S,et al. Pathogenesis of acute stroke and the role of inflammasomes[J]. Ageing Res Rev,2013,12(4):941-966. DOI:10. 1016/j. arr. 2013. 09. 004.
[4] Skaper SD,Facci L,Zusso M,et al. An Inflammation-centric view of neurological disease:beyond the neuron[J]. Front Cell Neurosci,2018,12:72. DOI:10. 3389/fncel. 2018. 00072.
[5] Shrivastava AK,Singh HV,Raizada A,et al. C-reactive protein,inflammation and coronary heart disease[J]. Egypt Heart J,2015,67(2):89-97. DOI:10. 1016/j. ehj. 2014. 11. 005.
[6] Toldo S,Mezzaroma E,O'Brien L,et al. Interleukin-18 mediates interleukin-1-induced cardiac dysfunction[J]. Am J Physiol Heart Circ Physiol,2014,306(7):H1025-H1031. DOI:10.1152/ajpheart. 00795. 2013.
[7] Ma JB,Chen L,Gao B,et al. Effect of polymorphisms in interleukin-18 gene on the susceptibility to coronary artery disease in a Chinese population[J]. Genet Mol Res,2016,15(4):gmr15048708. DOI:10. 4238/gmr15048708.
[8] Shi H,Leng S,Liang H,et al. Association study of C-reactive protein associated gene HNF1A with ischemic stroke in Chinese population[J]. BMC Med Genet,2016,17(1):51. DOI:10.1186/s12881-016-0313-3.
[9]韦广粤,陈军宁,富学林,等. IL-18基因启动子区-137G/C多态性与急性脑梗死关系的研究[J].广西医学,2013,35(6):675-677. DOI:10. 11675/j. issn. 0253-4304. 2013. 06. 04.
[10]任敦林,刘丽君,宋岩,等. IL-18基因启动子多态性与缺血性脑卒中关系[J].齐鲁医学杂志,2012,27(3):223-225.DOI:10. 3969/j. issn. 1008-0341. 2012. 03. 012.
[11]戴肖力,王占强.白细胞介素18基因启动子区-607 C/A多态性与缺血性卒中的相关性[J].河北医科大学学报,2014,35(6):681-683. DOI:10. 3969/j. issn. 1007-3205. 2014. 06.020.
[12] Liu Y,Geng PL,Yan FQ,et al. C-reactive protein-717A> G and-286C> T> A gene polymorphism and ischemic stroke[J]. Chin Med J(Engl),2015,128(12):1666-1670. DOI:10. 4103/0366-6999. 158371.