Abstract
BackgroundMyocardial apoptosis is closely related to myocardial injury caused by coronary microembolization (CME).Nuclear factor erythroid 2-like (Nrf2) has been taken into account as an inhibitor of apoptosis in various tissues. Thus, this research aims to investigate which part Nrf2/HO-1 signaling pathway plays in myocardial apoptosis process following the effect of CME on rats.MethodsSeparate 40 rats then form them into a group of shame, a group of CME, a group of CME plus AAV-Nrf2(AAV-Nrf2 (CME) group) and a group of CME plus AAV-control (AAV-control (CME) group) stochastically and averagely. Rat CME was established by injecting into the left ventricular chamber, with or without pretreatment of adeno-associated virus Nrf2 (AAV-Nrf2). Echocardiological measurements, using Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) to stain, conducting Quantitative PCR in real time (RT-PCR) as well as Western blotting to evaluate the impacts of them functionally, morphologically and molecularly in CME.ResultsNrf2 decreased in cardiomyocytes after CME. Upregulation of Nrf2 inside an organism through AAV connect to improving the function of heart as well as attenuating myocardial apoptosis, following the restrain of proapoptotic mRNAs and proteins like caspase-3, caspase-9 and bax expressing as well as the increase of antiapoptotic mRNA and proteins like HO-1 and bcl-2 expressing.ConclusionActivation of Nrf2/HO-1 pathway can improve CME-induced cardiac dysfunction effectively and also reduce the myocardial apoptosis.
Highlights
Myocardial apoptosis is closely related to myocardial injury caused by coronary microembolization (CME).Nuclear factor erythroid 2-like (Nrf2) has been taken into account as an inhibitor of apoptosis in various tissues
The results of this research emphasized the significant part that Nrf2/Heme oxygenase-1 (HO-1) plays in the pathogenesis of CME-connected myocardial dysfunction as well as in the apoptosis
We initially illuminate the part of Nrf2/HO-1 pathway plays in the CME model
Summary
Myocardial apoptosis is closely related to myocardial injury caused by coronary microembolization (CME).Nuclear factor erythroid 2-like (Nrf2) has been taken into account as an inhibitor of apoptosis in various tissues. This research aims to investigate which part Nrf2/HO-1 signaling pathway plays in myocardial apoptosis process following the effect of CME on rats. Liang et al BMC Cardiovascular Disorders (2017) 17:272 stress effects. In those HT22 cells, HO-1 is over expressed which confer antiapoptotic protective effects against H/R [12]. Nuclear factor erythroid 2-like (Nrf2) is a primary element of transcription. It adjusts numerous ways of apoptosis in a cell [13]. Recent studies have paid more attention to the Nrf2/HO-1 approach that is a key part in the apoptosis and that regulates and lowers the cardiomyocyte apoptosis [14]
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