Naringenin alleviates myocardial ischemia reperfusion injury by enhancing the myocardial miR-126-PI3K/AKT axis in streptozotocin-induced diabetic rats

xlomafota13 shared this article with you from Inoreader Naringenin alleviates myocardial ischemia reperfusion injury by enhancing the myocardial miR-126-PI3K/AKT axis in streptozotocin-induced diabetic rats Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):810. doi: 10.3892/etm.2021.10242. Epub 2021 May 27. ABSTRACT Ischemic heart disease (IHD) is a leading cause of death in patients with type 1 diabetes. The key to treating IHD is to restore blood supply to the ischemic myocardium, which inevitably causes myocardial ischemia reperfusion (MI/R) injury. Although naringenin (Nar) prevents MI/R injury, the role of Nar in diabetic MI/R (D-MI/R) injury remains to be elucidated. The PI3K/AKT signaling pathway and microRNA (miR)-126 have previously been shown to serve anti-MI/R injury roles. The present study aimed to investigate the protection of Nar against D-MI/R injury and the role of the miR-126-PI3K/AKT axis. Diabetic rats were treated distilled water or Nar (25 or 50 mg/kg, orally) for 30 days and then exposed to MI/R. The present results revealed that Nar alleviated MI/R injury in streptozotocin (STZ)-induced diabetic rats, as shown below: the reduction myoc ardial enzymes levels was measured using spectrophotometry, the increase of cardiac viability was detected by MTT assay, the inhibition of myocardial oxidative stress was measured using spectrophotometry and the enhancement of cardiac function were recorded using a hemodynamic monitoring system. Furthermore, Nar upregulated the myocardial miR-126-PI3K/AKT axis in D-MI/R rats. These results indicated that Nar alleviated MI/R injury through upregulating the myocardial miR-126-PI3K/AKT axis in STZ-induced diabetic rats. The current findings revealed that Nar, as an effective agent against D-MI/R injury, may provide an effective approach in the management of diabetic IHD. PMID:34093766 | PMC:PMC8170646 | DOI:10.3892/etm.2021.10242 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.