Ischaemic preconditioning-induced serum exosomes protect against myocardial ischaemia/reperfusion injury in rats by activating the PI3K/AKT signalling pathway
Ischemia / reperfusion (I / R) injury can cause severe arrhythmias and myocardial damage worsens. Exosomes are small membrane vesicles that play a protective role of injury I / R myocardium. This study aims to explore the protective effects of ischemic preconditioning (IPC) induced serum exosomes (IPC-Ex) on the injury I / R myocardium in rats and the underlying mechanism. serum exosomes derived from rats IPC and quantified using bicinchoninic acid assay kit. IPC-Exo (50 mg) injected into the myocardium infarction immediately after the ligation. Rats were randomly divided into Sham, I / R, IPC-Ex + I / R, I / R + LY294002, and I / R + group IPC-Ex + LY294002. hemodynamic parameters measured by physiological recording.
Transthoracic echocardiography is used to detect heart function. Serum levels of creatine kinase-MB isomers, lactate dehydrogenase, aspartate transaminase, tumor necrosis factor-alpha, interleukin (IL) -1β, and IL-10 were detected by enzyme-linked immunosorbent assay. Triphenyl tetrazolium chloride staining was used to measure the size of myocardial infarction. Apoptosis in myocardial tissue was detected by TUNEL staining. Western blotting was used to detect the level of PI3K / AKT and proteins associated with apoptosis.
The results of our study indicate that treatment with IPC-Ex improved heart function and reduce the production of inflammatory factors, cardiomyocyte apoptosis, and myocardial infarct size. In addition, the IPC-Ex treatment promoted protein expression of Bcl-2, p-PI3K and p-AKT but inhibited the caspase-3 and Bax. However, treatment with LY294002 significantly reverse the increase in p-PI3K and p-AKT levels, hemodynamic improvement, and decreased production of inflammatory factor and apoptosis in group I / R + IPC IPC-Exo-Exo-induced. Taken together, our results suggest that the IPC-Ex can reduce the injury I / R via activating PI3K / AKT signaling pathway.
Ischaemic preconditioning-induced serum exosomes protect against myocardial ischaemia/reperfusion injury in rats by activating the PI3K/AKT signalling pathway
Tanshinone IIA ameliorates the development of CAD Through Heart Settings H9c2 Cell Proliferation and Apoptosis by miR-133a-3p / EGFR Axis
Background: Coronary artery disease (CAD) leads to the world of death, serious threat to human health. Tanshinone IIA (Tan IIA), which can be extracted from Danshen, applied in the treatment of cardiovascular and cerebrovascular diseases. MicroRNAs (miRNAs, Mirs) plays an important role in cell proliferation and apoptosis of cells of the cardiovascular system. The purpose of this study was to explore the role of Tan IIA in CAD in vitro and the underlying molecular mechanisms.
Methods: Real-time polymerase chain reaction (RT-PCR) and Western blot used to detect miRNA / mRNA and protein, respectively. target genes miR-133a-3p searched at TargetScan and targeting relationships verified by dual-luciferase reporter assay. Cell proliferation was determined using cells Counting Kit-8 (CCK-8) and Edu labeling. Cell apoptosis was detected by flow cytometry and TUNEL staining.
Results: In this study, lower levels of miR-133a-3p and epidermal growth factor receptor that is higher (EGFR, the target of miR-133a-3p) level found in H2O2-induced cell H9c2. In addition, Tan IIA-regulated miR-133a-3p and downregulated the expression of EGFR. In addition, Tan IIA promoted cell proliferation and reduced apoptosis and increased G0 / G1, which is reversed with inhibitors of miR-133a-3p, while siRNA-EGFR eliminate the effects caused by miR-133a-3p in H2O2-induced cell H9c2.
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Conclusion: Tan IIA reversed H2O2-induced reduction of cell proliferation, induction of cell apoptosis and G0 / G1 arrest in the cell reduction H9c2 by miR-133a-3p / EGFR axis. The findings suggest a molecular basis Tan IIA potential in treating patients with CAD.
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