Key result
Puerarin attenuates Ang II-induced cardiac hypertrophy by blocking Rac1-dependent NADPH oxidase activation.
Why the study?
The effects of puerarin on angiotensin II-induced NADPH oxidase activation and oxidative stress-related signaling pathways in cardiomyocyte hypertrophy were unclear.
Does puerarin prevent Angiotensin II-induced cardiac hypertrophy in mouse models?
Does puerarin prevent Angiotensin II-induced cardiac hypertrophy in mouse models?
Puerarin suppresses Angiotensin II-induced cardiac hypertrophy in mice by inhibiting Rac1-dependent NADPH oxidase activation and AP-1 signaling.
Answers are grounded in this paper and cite their sources.
Puerarin effects on AngII-induced cardiomyocyte oxidative stress remain hypothesis-generating; further translational studies needed before clinical consideration.
PURPOSE: To examine the effects of puerarin (Pue) on angiotensin II (AngII)-induced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation and oxidative stress-related signaling pathways in the hypertrophic response of cardiomyocytes. METHODS: Primary cardiomyocytes of neonatal C57BL/6J mice were pretreated with Pue (50, 100 μmol/L) and were then stimulated with AngII 1 μmol/L. NADPH oxidase activity and reactive oxygen species (ROS) levels were measured by lucigenin-enhanced chemiluminescence assay and flow cytometry. Western blotting was used to detect the distribution of the oxidase subunits, extracellular signal-regulated kinase (ERK1/2) and c-jun N-terminal kinase (JNK1/2) activation, and an electrophoretic mobility shift assay (EMSA) was performed to analyze the DNA binding activity of activator protein-1 (AP-1). Adult C57BL/6J mice were infused with AngII and were administered with Pue (100, 200 mg·kg-1·d-1) for 15 d. After the treatment, systolic blood pressure (SBP) and left ventricular wall thickness were examined. The ratios of heart weight to body weight (HW/BW) and left ventricular weight to body weight (LVW/BW) were measured, and heart morphometry was assessed. RESULTS: In vitro, Pue dose-dependently blocked the phosphorylation of ERK1/2 and JNK1/2 and eventually abolished AP-1 binding activity through the inhibition of ROS production. Further studies revealed that AngII treatment resulted in increased NADPH oxidase activity, which was suppressed by Pue via the disruption of Rac1 activation and membrane translocation of oxidase subunits. In vivo, Pue attenuated cardiac hypertrophy, as evaluated by decreased HW/BW, LVW/BW, myocyte surface area, and left ventricular wall thickness. CONCLUSIONS: The anti-hypertrophic mechanism of Pue occurred by blocking Rac1-dependent NADPH oxidase activation and downstream redox-sensitive AP-1 signaling pathways.
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Gang et al. (2015) studied Cardiac hypertrophy (n=50). Puerarin vs. Angiotensin II alone (vehicle) was evaluated on Cardiac hypertrophy (assessed by HW/BW, LVW/BW, myocyte surface area, and left ventricular wall thickness) (p=<0.01). Puerarin significantly attenuated Angiotensin II-induced cardiac hypertrophy by blocking Rac1-dependent NADPH oxidase activation and downstream redox-sensitive AP-1 signaling pathways.
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