期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 60, 期 7, 页码 1850-1856出版社
AMER CHEMICAL SOC
DOI: 10.1021/jf204461z
关键词
delphinidin-3-glucoside; oxidized LDL; mitochondrial respiratory chain enzymes; NADPH oxidase; apoptosis; vascular endothelial cells
资金
- Canadian Diabetes Association
- Heart and Stroke Foundation of Manitoba
- Canadian Institutes of Health Research
Increased oxidative stress and apoptosis were detected in atherosclerotic lesions. Oxidized low-density lipoprotein (oLDL) may induce oxidative stress and apoptosis via multiple pathways in vascular endothelial cells (EC). Delphinidin-3-glucoside (D3G), an anthocyanidin glycan enriched in dark-skin berries, may neutralize those effects of oLDL in EC. The present study demonstrated that oLDL increased the generation of intracellular NADPH-dependent superoxide and impaired redox status in cultured porcine aortic EC (PAEC). The activities of mitochondrial respiratory chain complex I-IV and the contents of NADH dehydrogenase (ND)1, ND6 (complex I enzyme subunits), or cytochrome b (complex III enzyme subunit) were significantly reduced in PAEC treated with oLDL compared to controls. Treatment with oLDL significantly increased the abundances of NADPH oxidase (NOX)2, NOX4, and p22phox in PAEC. oLDL reduced cell viability and the protein content of B-cell lymphoma (Bcl)-2, but increased the content of caspase 3 in PAEC. Co-treatment with D3G prevented oLDL-induced increases in intracellular superoxide or in the protein content of NOX2, NOX4, p22phox, or caspase 3, inhibited the impairment of redox statues or cell viability, and prevented the attenuation of mitochondria] enzyme activities and the reductions of Bcl-2, ND1, or cytochrome b contents in PAEC. The findings suggest that oLDL induced oxidative stress and apoptosis in EC, which was associated with the activation of NOX, the impairment of mitochondria] respiration chain enzymes, and the disorder of key regulators for apoptosis. D3G neutralized the harmful effects of oLDL on oxidative stress, mitochondrial dysfunction, and apoptosis in cultured vascular EC.
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