Effect Of Auraptene Research Articles

Auraptene, a citrus peel-derived natural product, prevents myocardial infarction-induced heart failure by activating PPARα in rats

BackgroundAuraptene derived from the peel of Citrus hassaku possesses anti-tumor, anti-inflammatory, and neuroprotective activities. Thus, it could be a valuable pharmacological alternative to treat some diseases. However, the therapeutic value of auraptene for heart failure (HF) is unknown. Study design/methodsIn cultured cardiomyocytes from neonatal rats, the effect of auraptene on phenylephrine-induced hypertrophic responses and peroxisome proliferator-activated receptor-alpha (PPARα)-dependent gene transcriptions. To investigate whether auraptene prevents the development of heart failure after myocardial infarction (MI) in vivo, Sprague–Dawley rats with moderate MI (fractional shortening < 40%) were randomly assigned for treatment with low- or high-dose auraptene (5 or 50 mg/kg/day, respectively) or vehicle for 6 weeks. The effects of auraptene were evaluated by echocardiography, histological analysis, and the measurement of mRNA levels of hypertrophy, fibrosis, and PPARα-associated genes. ResultsIn cultured cardiomyocytes, auraptene repressed phenylephrine-induced hypertrophic responses, such as increases in cell size and activities of atrial natriuretic factor and endothelin-1 promoters. Auraptene induced PPARα-dependent gene activation by enhancing cardiomyocyte peroxisome proliferator-responsive element reporter activity. The inhibition of PPARα abrogated the protective effect of auraptene on phenylephrine-induced hypertrophic responses. In rats with MI, auraptene significantly improved MI-induced systolic dysfunction and increased posterior wall thickness compared to the vehicle. Auraptene treatment also suppressed MI-induced increases in myocardial cell diameter, perivascular fibrosis, and expression of hypertrophy and fibrosis response markers at the mRNA level compared with vehicle treatment. MI-induced decreases in the expression of PPARα-dependent genes were improved by auraptene treatment. ConclusionsAuraptene has beneficial effects on MI-induced cardiac hypertrophy and left ventricular systolic dysfunction in rats, at least partly due to PPARα activation. Further clinical studies are required to evaluate the efficacy of auraptene in patients with HF.

Comparison of Umbelliprenin and Auraptene in Cytotoxic Effects and Myeloid Cell Leukemia Type-1 (Mcl-1) Gene Expression

Induction of apoptosis in tumor cells is one of the mechanisms of chemotherapy. Myeloid cell leukemia type 1 is one of the Bcl-2 protein families that make an important role in chemo resistance to drugs. Thus down-regulation of myeloid cell leukemia type 1 gene is one of the aims in chemotherapy. Umbelliprenin and auraptene are naturally coumarins. Cytotoxicity and apoptosis induction is one of their effects. In this study we examined the cytotoxicity of these two coumarins against some cancerous cell lines by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay method and compare them together. In next step, we tested the effect of auraptene. On myeloid cell leukemia type 1 gene expression in Jurkat cells by real time polymerase chain reaction method. We found that umbelliprenin and auraptene. Have cytotoxic effect against cancerous cell lines. Auraptene is more cytotoxic than umbelliprenin. We also found that auraptene down-regulates myeloid cell leukemia type 1 gene expression in a pattern that different from umbelliprenin.

Suppressing effect of auraptene on human melanoma cells in vitro

Suppressing effect of auraptene on human melanoma cells in vitro