Mechanism of the hypoxia inducible factor 1/hypoxic response element pathway in rat myocardial ischemia/diazoxide post‑conditioning.

ABSTRACT: Ischemic post‑conditioning (IPO) and diazoxide post‑conditioning (DPO) has been proven to reduce myocardial ischemia reperfusion injury (MIRI); however, the mechanisms of IPO/DPO are still not clear. The present study aimed to investigate whether mitochondrial ATP‑sensitive potassium channels (mitoKATP) channels are activated by IPO/DPO, which may further activate the hypoxia inducible factor 1/hypoxic response element (HIF‑1/HRE) pathway to mitigate MIRI. Using a Langendorff perfusion device, healthy male (250‑300 g) Sprague Dawley rat hearts were randomly divided into the following groups. Group N was aerobically perfused with K‑H solution for 120 min. Group ischaemia/reperfusion (I/R) was aerobically perfused for 20 min, then subjected to 40 min hypoxia plus 60 min reperfusion. Group IP

SUBMITTER: Li J 

PROVIDER: S-EPMC7003038 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature