Abstract

<h3>Background</h3> Wnt and NF-κB signal pathway are all related to cardiac remodelling post-infarction and there were age-related differences of outcome post infarction. We study changes of these two signal pathways in heart in old mice to prepare some materials for advanced study. <h3>Methods</h3> We used 20 mice to study changes of these two signal pathways: 10 in young (3-mo) and old group (18-mo) respectively. They were detected expression of dvl-1, β-catenin, p/t GSK-3β and connexin 43 in the left ventricle (LV) by western-blot. And they were detected expression of p65 and p50 by immunohistochemistry and western-blot. At the same time they were detected expression of ICAM-1 and VCAM-1. <h3>Results</h3> (1) Expression of dvl-1 increased by 2.41 fold in old group compared with young mice in the LV (<i>P</i> = 0.000). There were no statistically differences of expression of β-catenin between the old and young group (<i>P</i> = 0.647) in LV. Ratio of p/t GSK-3β is much lower in old compared with young (<i>P</i> = 0.000). When talking about connexin 43, there were statistically significant differences in old group compared with young (<i>P</i> = 0.001) in the LV. (2) There was no difference of numbers of p65 and p50 positive cells between old and young group by immunohistochemistry (<i>P &lt;</i> 0.05). But expression of p65 and p50 in nuclear protein in old group is higher than it in young group (<i>P</i> = 0.000). There was no difference of ICAM-1 between old and young group (<i>P</i> = 0.401). Expression of VCAM-1 in old group was higher than it in young group (<i>P</i> = 0.000). <h3>Conclusions</h3> There were age-related differences of protein associated with Wnt and NF-κB signal pathway in heart. Progressing study about changes in these two signal pathway post myocardial-infarction might find new mechanisms about age-related differences of cardiac remodelling.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.