RESUMO
Rhynchophylline (RP), the primary active ingredient of Uncaria rhynchophylla, has an antihypertensive effect and protects against ischemiainduced neuronal damage. The present study aimed to examine the roles and mechanisms of RP in myocardial ischemiareperfusion (MI/R) injury of rat cardiomyocytes. Cell viability, reactive oxygen species, mitochondrial membrane potential (MMP) and cell apoptosis were examined by a Cell Counting Kit8 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/Rinduced cardiomyocytes, and suppressed the MI/Rinduced apoptosis of cardiomyocytes. Additionally, RP modulated the Ca2+ and MMP levels in MI/Rinduced cardiomyocytes. Furthermore, RP decreased the oxidative stress and mPTP level of MI/Rinduced cardiomyocytes. It was additionally observed that RP affected the apoptosisassociated protein expression and regulated the mitochondrialassociated gene expression in MI/Rinduced cardiomyocytes. In conclusion, RP ameliorated MI/R injury through the modulation of mitochondrial mechanisms. The potential effects of RP on the protection of MI/Rinduced apoptosis of cardiomyocytes suggest that RP may be an effective target for MI/R therapy.
Assuntos
Apoptose/efeitos dos fármacos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Oxindóis/farmacologia , Animais , Apoptose/genética , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Biomarcadores , Cálcio/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Expressão Gênica , Metaloproteinases da Matriz/metabolismo , Proteínas de Transporte da Membrana Mitocondrial/metabolismo , Poro de Transição de Permeabilidade Mitocondrial , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/etiologia , Estresse Oxidativo/efeitos dos fármacos , RatosRESUMO
OBJECTIVES: Epidemiological studies evaluating the association of nut consumption with coronary heart disease (CHD) risk have produced inconsistent results. The current study aimed to assess the CHD risk for the highest versus the lowest categories of nut consumption, the dose-response association of CHD for every 1 serving/week increment in nut consumption, and the heterogeneity among studies and publication bias. METHODS: Pertinent studies were identified by a search in PubMed and Web of Knowledge up to January 2014. A random-effect model was used to combine the results. The dose-response relationship was assessed by restricted cubic spline and variance-weighted least squares regression analysis. Publication bias was estimated using Egger's regression asymmetry test. RESULTS: Ten articles with 14 studies including 6302 CHD cases were included in this meta-analysis. Pooled results suggested that highest nut consumption amount versus lowest amount was associated significantly with a reduced risk of CHD [summary relative risk (RR)=0.681, 95% confidence interval (CI)=0.592-0.783, I(2)=62.7%], especially among USA (summary RR=0.671, 95% CI=0.591-0.761) and prospective studies (summary RR=0.660, 95% CI=0.581-0.748). A linear dose-response relationship was found, and the risk of CHD decreased by 10% for every 1 serving/week increase intake of nut (summary RR=0.90, 95% CI=0.87-0.94) No publication bias was found. CONCLUSION: Our analysis suggested that higher nut consumption might have a protective effect on CHD risk, especially in the USA, which needs to be confirmed.