Zhang Ming-Jie, Zhou Yi, Wang Xu, Chen Xue, Pi Yan, Guo Lu, Gao Chang-Yue, Li Jing-Cheng, Zhang Li-Li
Department of Neurology, Institute of Surgery Research, Daping Hospital, Third Military Medical University, 10 Changjiang Branch Road, Yuzhong District, Chongqing 400042, PR China.
Meta Gene. 2016 Jun 29;9:165-72. doi: 10.1016/j.mgene.2016.06.006. eCollection 2016 Sep.
Some epidemiological studies have evaluated the association between interleukin (IL)-18 promoter polymorphisms and the risk of ischemic stroke (IS), but the results were inconsistent. The present meta-analysis was therefore performed to investigate the relationship between IL-18 promoter 137G/C and 607C/A polymorphisms and the risk of IS in the Chinese population. Related studies from PubMed, Embase, Web of Science, CBMdisc and CNKI databases up to November 1, 2014 were systematically searched, also the reference lists of identified articles were manually searched. Information was extracted to calculate for the allelic, genotypic, dominant and recessive models using the pooled odds ratios (ORs) along with 95% confidence intervals (CIs). Evidence of significant association between 607C/A polymorphism and risk of IS was found in four genetic models based on the overall population. However, no significant association between 137G/C polymorphism and risk of IS was found in four genetic models. In summary, the present study suggests that IL-18 gene promoter 607A polymorphism is a protective factor for IS in the Chinese population, while 137C polymorphism has weaker or no protective properties. Still, a larger number of studies with large scale and sufficient original information are required to further confirm our findings.
一些流行病学研究评估了白细胞介素(IL)-18启动子多态性与缺血性中风(IS)风险之间的关联,但结果并不一致。因此,本荟萃分析旨在研究IL-18启动子137G/C和607C/A多态性与中国人群IS风险之间的关系。系统检索了截至2014年11月1日来自PubMed、Embase、Web of Science、CBMdisc和CNKI数据库的相关研究,同时还手动检索了已识别文章的参考文献列表。提取信息以使用合并优势比(OR)以及95%置信区间(CI)计算等位基因、基因型、显性和隐性模型。基于总体人群,在四种遗传模型中发现607C/A多态性与IS风险之间存在显著关联的证据。然而,在四种遗传模型中未发现137G/C多态性与IS风险之间存在显著关联。总之,本研究表明,IL-18基因启动子607A多态性是中国人群IS的保护因素,而137C多态性的保护作用较弱或无保护作用。尽管如此,仍需要更多大规模且原始信息充分的研究来进一步证实我们的发现。