It is currently accepted that the consumption of fruit-derived antioxidants such as vitamin C, carotenoids, and flavonoids provides a preventive effect against cardiovascular disease. The purpose of the present study was to investigate potential cardiovascular protective properties of aqueous and 70% ethanol extracts from kiwifruit by analyzing the antioxidative, antihypertensive, hypocholesterolemic, and fibrinolytic activities in vitro. Aqueous and 70% ethanol extracts at 50 mg/ml showed DPPH-radical scavenging activities of 72.31% and 70.75%, respectively. Total antioxidant activity in linoleic acid emulsion was 85-88% at 10 mg/ml and 96-98% at 50 mg/ml of kiwifruit extract. Inhibitory activities against angiogensin I-converting enzyme of kiwifruit extracts were 21-26% at 10 mg/ml and 46-49% at 50 mg/ml, and inhibitory activities on HMG-CoA reductase were 13-14% at 10 mg/ml and 19-30% at 50 mg/ml. Fibrinolytic activity of kiwifruit was also observed at a high concentration of 100 mg/ml in both aqueous and 70% EtOH extracts. Based on our results, kiwifruit have potential cardiovascular protective properties in vitro.

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The extract obtained from berries contains high amounts of anthocyanins, and this extract is used as a phytotherapeutic agent for different types of diseases. In this study, we examined the cytoprotective effects of cyanidin-3-glucoside (C3G) isolated from mulberry fruit against pancreatic β-cell apoptosis caused by hydrogen peroxide (H2O2)-induced oxidative stress. The MIN6 pancreatic β-cells were used to investigate the cytoprotective effects of C3G on the oxidative stress-induced apoptosis of cells. Cell viability was examined by MTT assay and lipid peroxidation was assayed by thiobarbituric acid (TBA) reaction. Immunofluorescence staining, flow cytometry and western blot analysis were also used to determine apoptosis and the expression of proteins associated with apoptosis. Our results revealed that H2O2 increased the rate of apoptosis by stimulating various pro-apoptotic processes, such as the generation of intracellular reactive oxygen species (ROS), lipid peroxidation, DNA fragmentation and caspase-3 activation. However, C3G reduced the H2O2-induced cell death in the MIN6N pancreatic β-cells. In addition, we confirmed that H2O2 activated mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK) and p38 MAPK. C3G inhibited the phosphorylation of ERK and p38 without inducing the phosphorylation of JNK. Furthermore, C3G regulated the intrinsic apoptotic pathway-associated proteins, such as proteins belonging to the Bcl-2 family, cytochrome c and caspase-3. Taken together, our results suggest that C3G isolated from mulberry fruit has potential for use as a phytotherapeutic agent for the prevention of diabetes by preventing oxidative stress-induced β-cell apoptosis.

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The present study investigated the cytoprotective effects of cyanidin‑3‑glucoside (C3G), isolated from mulberry fruits, on the glucotoxicity‑induced apoptosis of pancreatic β‑cells to evaluate the antidiabetic effects of this compound. MIN6N pancreatic β‑cells were used to investigate the cytoprotective effects of C3G. In addition, the effects of C3G on the glucotoxicity‑induced apoptosis of pancreatic β‑cells was evaluated using MTT assay, immunofluorescent staining, flow cytometric and western blot analyses. The pancreatic β‑cells cultured under high glucose conditions exhibited distinct apoptotic features. C3G decreased the generation of intracellular reactive oxygen species, DNA fragmentation and the rate of apoptosis. C3G also prevented pancreatic β‑cell apoptosis induced by high glucose conditions by interfering with the intrinsic apoptotic pathways. In addition, C3G treatment resulted in increased insulin secretion compared with treatment with high glucose only. In conclusion, the results of the present study suggested that C3G obtained from mulberry fruits may be a potential phytotherapeutic agent for the prevention of diabetes.