The Inhibitory Effect of WenxinKeli on H9C2 Cardiomyocytes Hypertrophy Induced by Angiotensin II through Regulating Autophagy Activity

Figures

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  Figure 1. Effect of WXKL on myocardial cytoskeletal proteins induced by AngII. (a) H9C2 cell cytoskeletal proteins. (b) Cell widths was measured by the Image Pro Plus software. (c) Cell lengths of each group of cells measured with the Image Pro Plus software (∗∗P < 0.01 versus ∗P < 0.05 versus control group; ▲▲P < 0.01 versus ▲P < 0.05 versus AngII).

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  Figure 2. Effect of WXKL on mTOR and MAPLC3A protein expression in AngII-induced cardiomyocytes. (a) The expression levels of mTOR and MAPLC3A protein. (b) The quantification of MAPLC3A in the 8 groups. (c) The quantification of LC3 II/I in the 8 groups. (d) The quantification of mTOR in the 8 groups. Each experiment was repeated three times (∗P < 0.05, ∗∗P < 0.01 versus control group; ▲▲P < 0.01 versus ▲P < 0.05 versus AngII group).

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  Figure 3. Effect of WXKL on the expression of the autophagy marker protein LC3 in AngII-induced cardiomyocytes. (a) (1–8) shows the staining of LC3 II, (b) (1–8) shows the nucleus, and (c) (1–8) shows the merged images (scale: 30 μm).

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  Figure 4. Transmission electron microscopy analysis of cardiomyocytes. (a) The control group (a1: 5000x, a2: 12,000x). (b) The AngII group (a1: 5000x, a2: 12,000x), the black housing showing autophagosomes surrounded by double membranes. (c) The AngII + 5 g/L + WXKL group (a1: 5000x, a2: 12,000x). Scale: 1 μm (a1, b1, and c1), 200 nm (a2, b2, and c2).

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  Figure 5. Effect of WXKL on the total amount of autophagosome in AngII-induced cardiomyocytes. (a) Fluorescence after FITC staining. The images of H9c2 cells showing the staining with FITC (A) (1–8), the nucleus (B) (1–8), and the merged images (C) (1–8). (b) The average fluorescence intensity of each group. Each experiment was repeated at least three times (∗P < 0.05 versus control group; ▲▲P < 0.01 versus ▲P < 0.05 versus AngII) (scale: 100 μm).

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  Figure 6. Effect of WXKL on the content of AngII-induced ATP. Cellular viability was measured using the CellTiter-Glo luminescent cell viability assay kit (∗P < 0.05 versus control group; ▲P < 0.05; ▲▲P < 0.01 versus AngII group).

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  Figure 7. Effect of WXKL on AngII-induced cardiomyocyte apoptosis. (a) Flow cytometry-based apoptosis assay for H9C2 cell. (b) The statistical quantification of cell apoptosis, triplicate experiments were conducted for each group (∗∗P < 0.01; ∗P < 0.05 versus control group; ▲cP < 0.01 versus AngII group).