Open Access

Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis

  • Authors:
    • Qiao‑Ji Qin
    • Li‑Qiang Cui
    • Peng Li
    • Yong‑Bin Wang
    • Xue‑Zhi Zhang
    • Ming‑Lei Guo
  • View Affiliations

  • Published online on: January 30, 2019     https://doi.org/10.3892/mmr.2019.9908
  • Pages: 2581-2590
  • Copyright: © Qin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Rhynchophylline (RP), the primary active ingredient of Uncaria rhynchophylla, has an anti‑hypertensive effect and protects against ischemia‑induced neuronal damage. The present study aimed to examine the roles and mechanisms of RP in myocardial ischemia‑reperfusion (MI/R) injury of rat cardiomyocytes. Cell viability, reactive oxygen species, mitochondrial membrane potential (MMP) and cell apoptosis were examined by a Cell Counting Kit‑8 assay and flow cytometry, respectively. An ELISA was performed to assess the expression of oxidative stress markers. Spectrophotometry was used to detect the degree of mitochondrial permeability transition pore (mPTP) openness. Western blotting and reverse transcription‑ quantitative polymerase chain reaction assays were used to evaluate the associated protein and mRNA expression, respectively. The present results demonstrated that RP increased the cell viability of MI/R‑induced cardiomyocytes, and suppressed the MI/R‑induced apoptosis of cardiomyocytes. Additionally, RP modulated the Ca2+ and MMP levels in MI/R‑induced cardiomyocytes. Furthermore, RP decreased the oxidative stress and mPTP level of MI/R‑induced cardiomyocytes. It was additionally observed that RP affected the apoptosis‑associated protein expression and regulated the mitochondrial‑associated gene expression in MI/R‑induced cardiomyocytes. In conclusion, RP ameliorated MI/R injury through the modulation of mitochondrial mechanisms. The potential effects of RP on the protection of MI/R‑induced apoptosis of cardiomyocytes suggest that RP may be an effective target for MI/R therapy.
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April-2019
Volume 19 Issue 4

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

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Spandidos Publications style
Qin QJ, Cui LQ, Li P, Wang YB, Zhang XZ and Guo ML: Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis. Mol Med Rep 19: 2581-2590, 2019.
APA
Qin, Q., Cui, L., Li, P., Wang, Y., Zhang, X., & Guo, M. (2019). Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis. Molecular Medicine Reports, 19, 2581-2590. https://doi.org/10.3892/mmr.2019.9908
MLA
Qin, Q., Cui, L., Li, P., Wang, Y., Zhang, X., Guo, M."Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis". Molecular Medicine Reports 19.4 (2019): 2581-2590.
Chicago
Qin, Q., Cui, L., Li, P., Wang, Y., Zhang, X., Guo, M."Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis". Molecular Medicine Reports 19, no. 4 (2019): 2581-2590. https://doi.org/10.3892/mmr.2019.9908