Diabetic cardiomyopathy (DCM), an independent coronary heart disease that develops in diabetic individuals, is characterized by changes in the myocardial structure and function. The aim of the present study was to investigate the protective effect of rutin on DCM in a streptozotocin-induced diabetic rat model. Rutin was orally administrated at a dose of 8 mg/kg body weight. Metabolic profiles, myocardial enzymes and oxidative stress were examined by biochemical tests. The expression levels of cellular proteins associated with apoptosis were measured by western blot analysis, while the levels of inflammatory factors were assessed by immunohistochemical analyses. Rats with DCM exhibited an abnormal metabolic profile, aberrant myocardial enzymes, elevation of oxidative stress markers, increased levels of inflammatory factors and enhanced apoptotic cell death. Notably, rutin was shown to protect and improve myocardial dysfunction, oxidative stress, apoptosis and inflammation in the hearts of the diabetic rats. In conclusion, these results indicated that rutin may have great therapeutic potential in the treatment of DCM, and possibly other cardiovascular disorders, by preventing oxidative stress, inflammation and cell death. However, further detailed studies are required to reveal the exact mechanisms underlying the protective effect of rutin.
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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