Co‑expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress.
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ABSTRACT: Myocardial ischemia/reperfusion (I/R) injury is a serious complication of reperfusion therapy for myocardial infarction. At present, there is not an effective treatment strategy available for myocardial I/R. The present study aimed to investigate the effects of human tissue kallikrein 1 (hTK1) and human tissue inhibitors of matrix metalloproteinase 1 (hTIMP1) gene co‑expression on myocardial I/R injury. A rat model of myocardial I/R injury and a cell model with hypoxia/reoxygenation (H/R) treatment in cardiac microvascular endothelial cells (CMVECs) were established, and treated with adenovirus (Ad)‑hTK1/hTIMP1. Following which, histological and triphenyl‑tetrazolium‑chloride staining assays were performed. Cardiac function was tested by echocardiographic measurement. The serum levels of o
SUBMITTER: Huang S
PROVIDER: S-EPMC7789088 | biostudies-literature | 2021 Feb
REPOSITORIES: biostudies-literature
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