Jin-Yu Liu1, Jie Shang2, Xiao-Dong Mu3, Zhi-Yong Gao4. 1. Department of Radiology, Yantai Yuhuangding Hospital, Yantai, 264000, PR China. 2. Department of Electrocardiogram, Yantai Yuhuangding Hospital, Yantai, 264000, PR China. 3. Clinical Laboratory, Yantai Yuhuangding Hospital, Yantai, 264000, PR China. 4. Department of Rehabilitation, Yantai Yuhuangding Hospital, Yantai, 264000, PR China. Electronic address: gzhiyong1@126.com.
Abstract
INTRODUCTION: Myocardial ischemia-reperfusion injury (MI/RI) is linked with serious inflammatory response, which may lead to myocyte injury. The important role of miR-27a in MI/RI has been previously demonstrated. Therefore, this study aims to investigate the effect of miR-27a targeting ABCA1 on MI/RI by investigating its influences on high thoracic epidural block (HTEB) mediated by the NF-κB signaling pathway. METHODS: A MI/RI mouse model and a MI/RI with HTEB mouse model were established to observed the histopathological changes and ultrastructure of myocardial tissues and assess the positive expression of ABCA1. Cardiac troponin T (cTnT), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined using enzyme-linked immunosorbent assay (ELISA). The expression of miR-27a, ABCA1, IκBα and p65 in myocardial cells that transfected with different mimic, inhibitor and siRNAs was determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot, with cell apoptosis analyzed by flow cytometry. RESULTS: ABCA1 was a target gene of miR-27a and was lowly expressed in myocardial tissues of MI/RI mice. The decreased content of cTnT, TNF-α and IL-1β and expression of miR-27a and p65 as well as increased expression of ABCA1 and IκBα were revealed in myocardial tissues of MI/RI mice with HTEB. miR-27a negatively regulated the expression of ABCA1, and inhibition of miR-27a could activated NF-κB pathway by up-regulating ABCA1 which contribute to suppressed myocardial cell apoptosis according to demonstration of elevated ABCA1 and IκBα, and decreased p65 in myocardial cell that transfected with miR-27a inhibitor. CONCLUSION: Collectively, our study indicates that inhibition of miR-27a could induce HTEB to protect mice against MI/RI by regulating ABCA1 and NF-κB signaling pathway.
INTRODUCTION: Myocardial ischemia-reperfusion injury (MI/RI) is linked with serious inflammatory response, which may lead to myocyte injury. The important role of miR-27a in MI/RI has been previously demonstrated. Therefore, this study aims to investigate the effect of miR-27a targeting ABCA1 on MI/RI by investigating its influences on high thoracic epidural block (HTEB) mediated by the NF-κB signaling pathway. METHODS: A MI/RI mouse model and a MI/RI with HTEB mouse model were established to observed the histopathological changes and ultrastructure of myocardial tissues and assess the positive expression of ABCA1. Cardiac troponin T (cTnT), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined using enzyme-linked immunosorbent assay (ELISA). The expression of miR-27a, ABCA1, IκBα and p65 in myocardial cells that transfected with different mimic, inhibitor and siRNAs was determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot, with cell apoptosis analyzed by flow cytometry. RESULTS: ABCA1 was a target gene of miR-27a and was lowly expressed in myocardial tissues of MI/RI mice. The decreased content of cTnT, TNF-α and IL-1β and expression of miR-27a and p65 as well as increased expression of ABCA1 and IκBα were revealed in myocardial tissues of MI/RI mice with HTEB. miR-27a negatively regulated the expression of ABCA1, and inhibition of miR-27a could activated NF-κB pathway by up-regulating ABCA1 which contribute to suppressed myocardial cell apoptosis according to demonstration of elevated ABCA1 and IκBα, and decreased p65 in myocardial cell that transfected with miR-27a inhibitor. CONCLUSION: Collectively, our study indicates that inhibition of miR-27a could induce HTEB to protect mice against MI/RI by regulating ABCA1 and NF-κB signaling pathway.