Abstract
Background: Inflammatory cells infiltrate into the ischemic and hypoxic myocardial tissue after myocardial infarction. B cells gather at the site of myocardial injury and secrete cytokines to regulate immune inflammation and fiber repair processes.Methods: The animal experiment intended to use ligation of the left anterior descending branch of C57BL/6 mice to establish a mice AMI model to observe the changes of activated B cells and cytokines at different time points. 88 12-week-old C57BL/6 male mice were divided into the Sham group (24 mice) and acute myocardial infarction (AMI ) group (64 mice) randomly. Besides, C57BL/6 Bmi-1 knock out (BKO) mice and C57BL/6 wild-type (WT) mice were used to establish AMI models to observe the expression levels of cardiomyocyte factors including TNF-α and IL-1β, IL-6, TGF-β1, COL1-A1, COL3-A1, TIMP-1, and MMP9. Moreover, pathological and collagen changes in the myocardium were analyzed. One-way ANOVA analysis of variance was used for comparison between multiple groups, and the LSD method was used for pairwise comparison between groups. P < 0.05 indicated statistical differences.Results: AMI model of C57BL/6 mice was established successfully. The ratio of activated B cells and expression of TNF-α, IL-1β, IL-6, TGF-β1, and BAFF in 5 days subgroup was highest in the myocardium, spleen, and peripheral blood with the most obvious myocardial inflammatory cells infiltration. mRNA expression levels of TNF-α, IL-1β, IL-6, TGF-β1 in 5 days subgroup of the BKO group were decreased compared with the WT group (P < 0.05). Among 2 weeks subgroups of Sham, WT, and BKO groups, the LVEDd and LVESd in the BKO and WT groups were less than those in the Sham group (P < 0.05). The LVEDd and LVESd of the BKO group were less than the WT group,EF was higher than the WT group (P < 0.05).Conclusion: Activated B cells participated in the sustained state of myocardial inflammation and immune system activation after AMI via promoting the secretion of cytokines, and may affect the metabolism of myocardial collagen. Moreover, B cells could damage the heart structure and left ventricular ejection function by promoting the expression of myocardial collagen Type I and type III.
The expression levels of plasma dimethylglycine (DMG), human maternally expressed gene 3 (MEG3), and Apelin-12 in patients with acute myocardial infarction and their clinical significance
