Programmed cell death

Cell biology

Flow cytometry

Molecular biology

Mitochondrial permeability transition pore

Biology

Reactive oxygen species

Endocrinology

Apoptosis

Ischemia

Membrane potential

Biochemistry

Dopamine

Dopaminergic

Oxidative stress

Internal medicine

Pharmacology

MPTP

Medicine

Chemistry

Cell

Reperfusion injury

Viability assay

Molecular Medicine Reports

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.

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