Propofol Protects Rat Cardiomyocytes from Anthracycline-Induced Apoptosis by Regulating MicroRNA-181a In Vitro and In Vivo

Figure 4

miR-181a contributes to reducing ADM-induced cardiomyocyte apoptosis by repressing Bcl-2. (a) RNAs isolated from H9c2 cells transfected with miR-181a inhibitor or control were analyzed by RT-qPCR to access the levels of miR-181a. The expression of miR-181a was reduced by miR-181a inhibitor transfection. (b) The cell viability of H9c2 cells transfected with miR-181a inhibitor or control in different treatment was tested by MTT assay. (c-e) After 24 h exposure of ADM treatment, the proportion of apoptotic cells was decreased in miR-181a inhibitor cells compared with control cells (). (d-f) The silencing of miR-181a in H9c2 cell treatment with ADM resulted in increased Bcl-2 () and decreased Bax () protein levels. (g) Rat Bcl-2 has strong rno-miR-181a-binding sites at its 3-UTR. MiR-181a seed pairing in the target regions is shown as vertical lines. (h) Relative luciferase activity was analyzed after wild-type or mutant Bcl-2-3UTR reporter plasmids were cotransfected with miR-181a mimic in H9c2 cells as shown. Compared to the negative control, miR-181a repressed the activity of luciferase fused to the WT Bcl-2-3UTR (), while it failed to repress the mutated one (). Data are representative of three independent experiments. Data from triplicate experiments were showed as mean ± SD (). The statistical analysis was performed with Student’s t-test. ; ; .

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