Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 mitochondrial 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 mitochondrial 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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PMID:Influence of delphinidin-3-glucoside on oxidized low-density lipoprotein-induced oxidative stress and apoptosis in cultured endothelial cells. 2227 27

Reactive oxygen species (ROS) play a pivotal role in the development of pathological cardiac hypertrophy. Delphinidin, a natural flavonoid, was reported to exert marked antioxidative effects. Therefore, we investigated whether delphinidin ameliorates pathological cardiac hypertrophy via inhibiting oxidative stress. In this study, male C57BL/6 mice were treated with DMSO or delphinidin after surgery. Neonatal rat cardiomyocytes (NRCMs) were treated with angiotensin II (Ang II) and delphinidin in vitro. Eighteen-month-old mice were administered delphinidin to investigate the effect of delphinidin on aging-related cardiac hypertrophy. Through analyses of hypertrophic cardiomyocyte growth, fibrosis and cardiac function, delphinidin was demonstrated to confer resistance to aging- and transverse aortic constriction (TAC)-induced cardiac hypertrophy in vivo and attenuate Ang II-induced cardiomyocyte hypertrophy in vitro by significantly suppressing hypertrophic growth and the deposition of fibrosis. Mechanistically, delphinidin reduced ROS accumulation upon Ang II stimulation through the direct activation of AMP-activated protein kinase (AMPK) and subsequent inhibition of the activity of Rac1 and expression of p47phox. In addition, excessive levels of ERK1/2, P38 and JNK1/2 phosphorylation induced by oxidative stress were abrogated by delphinidin. Delphinidin was conclusively shown to repress pathological cardiac hypertrophy by modulating oxidative stress through the AMPK/NADPH oxidase (NOX)/mitogen-activated protein kinase (MAPK) signaling pathway.
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PMID:Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway. 3220 25