Open Access

Icariin attenuates angiotensin II‑induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species‑dependent JNK and p38 pathways

  • Authors:
    • Heng Zhou
    • Yuan Yuan
    • Yuan Liu
    • Wei Deng
    • Jing Zong
    • Zhou‑Yan Bian
    • Jia Dai
    • Qi‑Zhu Tang
  • View Affiliations

  • Published online on: March 4, 2014     https://doi.org/10.3892/etm.2014.1598
  • Pages: 1116-1122
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Abstract

Icariin, the major active component isolated from plants of the Epimedium family, has been reported to have potential protective effects on the cardiovascular system. However, it is not known whether icariin has a direct effect on angiotensin II (Ang II)‑induced cardiomyocyte enlargement and apoptosis. In the present study, embryonic rat heart‑derived H9c2 cells were stimulated by Ang II, with or without icariin administration. Icariin treatment was found to attenuate the Ang II‑induced increase in mRNA expression levels of hypertrophic markers, including atrial natriuretic peptide and B‑type natriuretic peptide, in a concentration‑dependent manner. The cell surface area of Ang II‑treated H9c2 cells also decreased with icariin administration. Furthermore, icariin repressed Ang II‑induced cell apoptosis and protein expression levels of Bax and cleaved‑caspase 3, while the expression of Bcl‑2 was increased by icariin. In addition, 2',7'‑dichlorofluorescein diacetate incubation revealed that icariin inhibited the production of intracellular reactive oxygen species (ROS), which were stimulated by Ang II. Phosphorylation of c‑Jun N‑terminal kinase (JNK) and p38 in Ang II‑treated H9c2 cells was blocked by icariin. Therefore, the results of the present study indicated that icariin protected H9c2 cardiomyocytes from Ang II‑induced hypertrophy and apoptosis by inhibiting the ROS‑dependent JNK and p38 pathways.
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May-2014
Volume 7 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhou H, Yuan Y, Liu Y, Deng W, Zong J, Bian ZY, Dai J and Tang QZ: Icariin attenuates angiotensin II‑induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species‑dependent JNK and p38 pathways. Exp Ther Med 7: 1116-1122, 2014.
APA
Zhou, H., Yuan, Y., Liu, Y., Deng, W., Zong, J., Bian, Z. ... Tang, Q. (2014). Icariin attenuates angiotensin II‑induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species‑dependent JNK and p38 pathways. Experimental and Therapeutic Medicine, 7, 1116-1122. https://doi.org/10.3892/etm.2014.1598
MLA
Zhou, H., Yuan, Y., Liu, Y., Deng, W., Zong, J., Bian, Z., Dai, J., Tang, Q."Icariin attenuates angiotensin II‑induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species‑dependent JNK and p38 pathways". Experimental and Therapeutic Medicine 7.5 (2014): 1116-1122.
Chicago
Zhou, H., Yuan, Y., Liu, Y., Deng, W., Zong, J., Bian, Z., Dai, J., Tang, Q."Icariin attenuates angiotensin II‑induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species‑dependent JNK and p38 pathways". Experimental and Therapeutic Medicine 7, no. 5 (2014): 1116-1122. https://doi.org/10.3892/etm.2014.1598