Open Access

Icariside II ameliorates myocardial ischemia and reperfusion injury by attenuating inflammation and apoptosis through the regulation of the PI3K/AKT signaling pathway

  • Authors:
    • Bing‑Feng Guan
    • Xiao‑Feng Dai
    • Qi‑Bin Huang
    • Di Zhao
    • Jin‑Long Shi
    • Cheng Chen
    • Yan Zhu
    • Fen Ai
  • View Affiliations

  • Published online on: July 31, 2020     https://doi.org/10.3892/mmr.2020.11396
  • Pages: 3151-3160
  • Copyright: © Guan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Icariside II (ICAII) is a bioflavonoid compound which has demonstrated anti‑oxidative, anti‑inflammatory and anti‑apoptotic biological activities. However, to the best of our knowledge, whether ICAII can alleviate myocardial ischemia and reperfusion injury (MIRI) remains unknown. The aim of the present study was to determine whether ICAII exerted a protective effect on MIRI and to investigate the potential underlying mechanism of action. A rat MIRI model was established by ligation of the left anterior descending coronary artery for 30 min, followed by a 24 h reperfusion. Pretreatment with ICAII with or without a PI3K/AKT inhibitor was administered at the beginning of reperfusion. Morphological and histological analyses were detected using hematoxylin and eosin staining; the infarct size was measured using Evans blue and 2,3,5‑triphenyltetrazolium chloride staining; and plasma levels of lactate dehydrogenase (LDH) and creatine kinase‑myocardial band (CK‑MB) were analyzed using commercialized assay kits. In addition, the cardiac function was evaluated by echocardiography and the levels of cardiomyocyte apoptosis were determined using a TUNEL staining. The protein expression levels of Bax, Bcl‑2, cleaved caspase‑3, interleukin‑6, tumor necrosis factor‑α, PI3K, phosphorylated (p)‑PI3K, AKT and p‑AKT were analyzed using western blotting analysis. ICAII significantly reduced the infarct size, decreased the release of LDH and CK‑MB and improved the cardiac function induced by IR injury. Moreover, ICAII pretreatment significantly inhibited myocardial apoptosis and the inflammatory response. ICAII also upregulated the expression levels of p‑PI3K and p‑AKT. However, the protective effects of ICAII were abolished by an inhibitor (LY294002) of the PI3K/AKT signaling pathway. In conclusion, the findings of the present study suggested that ICAII may mitigate MIRI by activating the PI3K/AKT signaling pathway.
View Figures
View References

Related Articles

Journal Cover

October-2020
Volume 22 Issue 4

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Guan BF, Dai XF, Huang QB, Zhao D, Shi JL, Chen C, Zhu Y and Ai F: Icariside II ameliorates myocardial ischemia and reperfusion injury by attenuating inflammation and apoptosis through the regulation of the PI3K/AKT signaling pathway. Mol Med Rep 22: 3151-3160, 2020
APA
Guan, B., Dai, X., Huang, Q., Zhao, D., Shi, J., Chen, C. ... Ai, F. (2020). Icariside II ameliorates myocardial ischemia and reperfusion injury by attenuating inflammation and apoptosis through the regulation of the PI3K/AKT signaling pathway. Molecular Medicine Reports, 22, 3151-3160. https://doi.org/10.3892/mmr.2020.11396
MLA
Guan, B., Dai, X., Huang, Q., Zhao, D., Shi, J., Chen, C., Zhu, Y., Ai, F."Icariside II ameliorates myocardial ischemia and reperfusion injury by attenuating inflammation and apoptosis through the regulation of the PI3K/AKT signaling pathway". Molecular Medicine Reports 22.4 (2020): 3151-3160.
Chicago
Guan, B., Dai, X., Huang, Q., Zhao, D., Shi, J., Chen, C., Zhu, Y., Ai, F."Icariside II ameliorates myocardial ischemia and reperfusion injury by attenuating inflammation and apoptosis through the regulation of the PI3K/AKT signaling pathway". Molecular Medicine Reports 22, no. 4 (2020): 3151-3160. https://doi.org/10.3892/mmr.2020.11396