摘要
目的:探讨IL-32在大鼠心肌细胞缺氧损伤中的作用及其机制。方法:构建乳鼠心肌细胞缺氧模型后,比较缺氧组与正常组IL-32、IL-1β、IL-6、IL-18、TNF-α和IL-10 mRNA及蛋白水平的表达情况,以及IL-32与各细胞因子间的相关性。结果:与正常组相比,缺氧组心肌细胞坏死明显;IL-32、IL-1β、IL-6、IL-18、TNF-α和IL-10基因及蛋白表达水平均明显升高;Pearson相关分析提示IL-32与IL-1β、IL-6、IL-18、TNF-α和IL-10水平呈正相关。结论:大鼠心肌细胞缺氧后,IL-32表达水平明显升高;IL-32与传统细胞因子IL-1β、IL-6、IL-18、TNF-α和IL-10表达水平呈正相关。
Objective： To investigate the roles and mechanisms of interleukin-32 （IL-32） on rat cardiomyo- cytes with hypoxia injury. Methods： When eardiomyocytes with hypoxia injury was produced, mRNA and protein levels of IL-32, IL-1 [3, IL-6, IL-18, TNF-α and IL-10 were compared between hypoxia group and control group. The relationships of IL-32 with other factors were also evaluated. Results： When compared with control group, number of apoptotic cardiomyocytes was significantly higher, accompanied with higher levels of mRNA and proteins of IL-32, IL-1β, IL-6, IL-18, TNF-α and IL-10. As indicated by the Pearson correlation analysis, IL-32 was pos- itively correlated with IL-113, IL-6, IL-18, TNF-α and IL-10. Conclusion： 1L-32 was significantly increased after insulted by hypoxia injury in rat eardiomyocytes, and IL-32 was positively correlated with inflammatory factors such as IL-1β, IL-6, IL-1β, TNF-α and IL-IO.
出处
《新医学》
2013年第4期282-284,共3页
Journal of New Medicine
基金
2012年深圳市科技计划项目(201203048)
