OBJECTIVES: Myocardial I/R injury is one of the most serious complications after reperfusion therapy in patients with myocardial infarction. Remifentanil has been found to protect the heart against I/R injury. However, its underlying mechanism remains uncertain in myocardial I/R injury. METHODS: The myocardial I/R injury rat model was established by 30 min of ischaemia followed by 24 h of reperfusion. The animal model was evaluated by the levels of TC, ALT and AST and H&E staining. The binding of miR-206-3p and TLR4 was predicted and verified using TargetScan software, luciferase reporter and RNA pull-down assays. The functional role and mechanism of remifentanil were identified by ultrasonic echocardiography, oxidative stress markers, H&E, Masson and TUNEL staining and western blot. KEY FINDINGS: The rat myocardial I/R injury model displayed a significantly high level of TC, ALT, AST, TLR4, p-IκBα and p-p65 and the presence of disorganized cells and inflammatory cell infiltration. The model also showed increased levels of LVEDD, LVESD, MDA, fibrosis and apoptosis and decreased levels of EF, FS, SOD and GSH, which were reversed with remifentanil treatment. Knockdown of miR-206-3p damaged cardiac function and aggravated oxidative stress. miR-206-3p could directly bind to TLR4. TLR4 overexpression destroyed cardiac function, exacerbated oxidative stress, increased levels of p-IκBα and p-p65 and aggravated pathology manifestation affected by remifentanil. CONCLUSIONS: Our results elucidated that remifentanil alleviated myocardial I/R injury by miR-206-3p/TLR4/NF-κB signalling axis.
OBJECTIVES: Myocardial I/R injury is one of the most serious complications after reperfusion therapy in patients with myocardial infarction. Remifentanil has been found to protect the heart against I/R injury. However, its underlying mechanism remains uncertain in myocardial I/R injury. METHODS: The myocardial I/R injury rat model was established by 30 min of ischaemia followed by 24 h of reperfusion. The animal model was evaluated by the levels of TC, ALT and AST and H&E staining. The binding of miR-206-3p and TLR4 was predicted and verified using TargetScan software, luciferase reporter and RNA pull-down assays. The functional role and mechanism of remifentanil were identified by ultrasonic echocardiography, oxidative stress markers, H&E, Masson and TUNEL staining and western blot. KEY FINDINGS: The rat myocardial I/R injury model displayed a significantly high level of TC, ALT, AST, TLR4, p-IκBα and p-p65 and the presence of disorganized cells and inflammatory cell infiltration. The model also showed increased levels of LVEDD, LVESD, MDA, fibrosis and apoptosis and decreased levels of EF, FS, SOD and GSH, which were reversed with remifentanil treatment. Knockdown of miR-206-3p damaged cardiac function and aggravated oxidative stress. miR-206-3p could directly bind to TLR4. TLR4 overexpression destroyed cardiac function, exacerbated oxidative stress, increased levels of p-IκBα and p-p65 and aggravated pathology manifestation affected by remifentanil. CONCLUSIONS: Our results elucidated that remifentanil alleviated myocardial I/R injury by miR-206-3p/TLR4/NF-κB signalling axis.