Abstract
Objective To investigate the effects of HOX transcript antisense RNA (HOTAIR) and miR-138 on inflammatory response and oxidative stress (OS) induced by IRI in rat cardiomyocytes. Methods H9C2 cells were divided into the control group, H/R group, H/R+siRNA NC group, H/R+si-HOTAIR group, and H/R+si-HOTAIR+inhibitor group. Expression levels of HOTAIR, miR-138, and inflammatory factors were detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The double luciferase reporter gene assay was used to detect the targeting relationship between HOTAIR and miR-138. Results Compared with the control group, the level of miR-138 and SOD in the H/R group was obviously reduced, while the expression levels of the HOTAIR, MDA, and NF-κB pathway were obviously increased. Compared with the H/R group, the level of miR-138 and SOD in the H/R+si-HOTAIR group was obviously increased, and the expression levels of the HOTAIR, MDA, and NF-κB pathway were obviously decreased. Compared with the H/R+si-HOTAIR group, the level of SOD in the H/R+si-HOTAIR+inhibitor group decreased; MDA content and the NF-κB pathway expression level increased. In the double luciferase reporter gene assay, compared with the HOTAIR wt+NC group, the luciferase activity of the HOTAIR wt+miR-138 mimic group was obviously decreased. Conclusions Silent HOTAIR can promote the expression of miR-138 and inhibit H/R-induced inflammatory response and OS by regulating the NF-κB pathway, thus protecting cardiomyocytes.
Highlights
Acute myocardial infarction (AMI) is the acute manifestation of coronary heart disease and the main cause of death
The H/R+si-HOX transcript antisense RNA (HOTAIR)+inhibitor group was cotransfected with si-HOTAIR and miR-138 inhibitor according to the instructions of Lipofectamine 2000 transfection agents
The results of immunofluorescence staining showed that the expression of SOD1 in the H/R group was obviously reduced
Summary
Acute myocardial infarction (AMI) is the acute manifestation of coronary heart disease and the main cause of death. If blood flow to the occluded vessels does not return, myocardial tissue in the infarct-related area will die Reperfusion strategies, such as drug thrombolysis, percutaneous coronary intervention, and coronary artery bypass grafting, are conducive to the early opening of occluded blood vessels, effectively saving ischemic myocardial tissue, reducing infarction area, and improving cardiac function, and have greatly improved the prognosis of patients [2]. As the study of myocardial ischemia reperfusion proceeds further, the researchers found that the reperfusion therapy can make the ischemia heart regain the blood perfusion in a short period of time to limit infarct area expansion, and many other benefits, it leads to myocardial ischemia reperfusion treatment itself after more serious dysfunction and structural damage; this phenomenon is called myocardial ischemia reperfusion injury (MIRI) [3, 4]. How to reduce MIRI has become the focus and hot topic of research in the field of coronary heart disease
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