Targeting the PI3K/STAT3 axis modulates age-related differences in macrophage phenotype in rats with myocardial infarction.

ABSTRACT: Ageing is associated with impaired repair mechanisms in cardiovascular diseases. Macrophages contribute to cardiac fibrosis after myocardial infarction (MI). The phosphatidyl-inositol-3-kinase (PI3K) pathway has been shown to play a role in cardiac remodelling after MI. It remained unclear whether n-butylidenephthalide, a major component of Angelica sinensis, can attenuate cardiac fibrosis by regulating the PI3K/signal transducer and activator of transcription 3 (STAT3)-mediated macrophage phenotypes in ageing rats after MI. Twenty-four hours after ligation of the left anterior descending artery, young (2-month-old) and ageing (18-month-old) male Wistar rats were treated with either vehicle or n-butylidenephthalide for 4 weeks. There were similar infarct sizes in both age groups. Compared

SUBMITTER: Lin CC 

PROVIDER: S-EPMC6714172 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature