Phenylethanol Glycosides Protect Myocardial Hypertrophy Induced by Abdominal Aortic Constriction via ECE‐1 Demethylation Inhibition and PI3K/PKB/eNOS Pathway Enhancement

Figures

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  Figure 1. (a) Echinacoside and (b) acteoside. (c) HPLC analysis of CPhGs.

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  Figure 2. Effects of CPhGs on cardiac ultrasound parameters in rats after AAC: (a) left ventricular posterior wall thickness (LVPWT); (b) left ventricular end-diastolic diameter (LVED); (c) left ventricular ejection fractions (LVEF); and (d) left ventricular fractional shortening (LVFS). ∗∗p < 0.01 versus sham; #p < 0.05, ##p < 0.01 versus AAC; ΔP < 0.05 versus AV (n = 9‐10).

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  Figure 3. Effects of CPhGs on HWI, CSAC, and fibrosis area in rats after AAC. (a) Heart shape, bar = 1 cm; (b) masson staining of rat myocardium, bar = 200 μm; and (c) HE staining of rat myocardium, bar = 50 μm; (d–g) heart weight (HW), heart weight index (HWI), fibrosis area, and cross-sectional area of cardiomyocytes (CSAC). ∗∗P < 0.01 versus sham; #P < 0.05, ##P < 0.01 versus AAC; ΔP < 0.05, ΔΔP < 0.01 versus AV (n = 9‐10).

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  Figure 4. Effect of CPhGs on the expression of myocardial hypertrophy gene mRNA in myocardial tissue of rats after AAC. ∗∗P < 0.01 versus sham; ##P < 0.01 versus AAC; ΔΔP < 0.01 versus AV (n = 9-10).

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  Figure 5. Effect of CPhGs on proinflammatory factor levels in plasma of rats after AAC. (a) Cyclooxygenase 1 (COX-1); (b) interleukin 6 (IL-6); (c) interleukin 1β (IL-1β); and (d) tumor necrosis factor α (TNF-α). ∗∗P < 0.01 versus sham. ∗∗P < 0.01 versus sham. #P < 0.01, ##P < 0.01 versus AAC. ΔP < 0.01, ΔΔP < 0.01 versus AV (n = 9-10).

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  Figure 6. Effects of CPhGs on the expression of COX‐2 and HMGB‐1 proteins in myocardial tissues of rats after AAC. (a) Cyclooxygenase 2 (COX‐2) and (b) high mobility group protein B1 (HMGB‐1). ∗∗P < 0.01 versus sham. #P < 0.05. ##P < 0.01 versus AAC. ΔP < 0.05, ΔΔP < 0.01 versus AV (n = 6).

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  Figure 7. Effect of CPhGs on the demethylation level of ECE-1 gene in myocardial tissue of rats after AAC. M: means methylation level, U: means demethylation level. ∗∗P < 0.01 versus sham, #P < 0.05, ##P < 0.01 versus AAC, and ΔP < 0.05 versus AV (n = 6).

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  Figure 8. Effect of CPhGs on the expression of ECE-1 in myocardial tissue of rats after AAC. (a), (b) ECE-1 protein level; (c) ECE-1 mRNA expression; and (d), (e) immunohistochemistry of ECE-1 in myocardial tissue. Bar = 20 μm. ∗∗P < 0.01 versus sham;#P < 0.05, ##P < 0.01 versus AAC; ΔP < 0.05, ΔΔP < 0.01 versus AV. (n = 6).

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  Figure 9. Effect of CPhGs on plasma ET-1 levels in rats after AAC. ∗∗P < 0.01 versus sham, ##P < 0.01 versus AAC, ΔΔP < 0.01 versus AV (n = 9‐10).

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  Figure 10. Effect of CPhGs on the expression of PI3K/PKB/eNOS pathway in myocardial tissue of rats after AAC. (a) p-PI3K protein level; (b) p-PKB protein level; and (c) p-eNOS protein level. ∗∗P < 0.01 versus sham, #P < 0.05, ##P < 0.01 versus AAC, ΔP < 0.05 versus AV. (n = 6).