Open Access

Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy

  • Authors:
    • Bin Ni
    • Donglai Zhou
    • Yunyan Jing
    • Shanxin Liu
  • View Affiliations

  • Published online on: August 17, 2018     https://doi.org/10.3892/mmr.2018.9399
  • Pages: 3649-3656
  • Copyright: © Ni et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Myocardial infarction (MI) is life‑threatening and is generally accompanied by myocardial hypertrophy. Notably, Hydroxysafflor yellow A (HSYA) can prevent tissue injuries. The objective of this study was to investigate the effect of HSYA on hypertrophy after MI. Hematoxylin and eosin (H&E) staining assays were performed to measure cell area. The protein synthesis rate was assessed using the 3H Leucine incorporation assay. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and the immunohistochemical assay were used to detect the expression of target genes. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and the reactive oxygen species (ROS) generation were examined using commercial kits. Decreased myocardial hypertrophy was observed in animals treated with HSYA. Furthermore, the expression of nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) was higher in HSYA administration groups compared with that in the MI model group. In H9c2 cardiomyocytes, the pretreatment with HSYA increased the cell viability, however, it reduced protein synthesis rate, mitigated cell surface area and decreased the expression of Brain natriuretic factor (BNP) and β‑myosin heavy chain (β‑MHC). By contrast, the downregulation of Nrf2 deteriorated and reversed the effect of Ang II and HSYA. Furthermore, oxidative stress was alleviated by HSYA via inhibiting ROS generation, modulating the activities of SOD and MDA. In addition, the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) and heme oxygenase‑1 (HO‑1) were recovered by the pretreatment of HSYA that was combated by siNrf2. In conclusion, HSYA exerted anti‑hypertrophic effects, which was pertinent with the activation of Nrf2/NQO‑1/HO‑1 signaling pathway. The findings of this study may inspire a novel strategy to combat MI.
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October-2018
Volume 18 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Ni B, Zhou D, Jing Y and Liu S: Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy. Mol Med Rep 18: 3649-3656, 2018.
APA
Ni, B., Zhou, D., Jing, Y., & Liu, S. (2018). Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy. Molecular Medicine Reports, 18, 3649-3656. https://doi.org/10.3892/mmr.2018.9399
MLA
Ni, B., Zhou, D., Jing, Y., Liu, S."Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy". Molecular Medicine Reports 18.4 (2018): 3649-3656.
Chicago
Ni, B., Zhou, D., Jing, Y., Liu, S."Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy". Molecular Medicine Reports 18, no. 4 (2018): 3649-3656. https://doi.org/10.3892/mmr.2018.9399