Nifedipine protects against overproduction of superoxide anion by monocytes from patients with systemic sclerosis.
作者： Yannick Allanore , Didier Borderie , Axel Périanin , Hervé Lemaréchal , Ohvanesse Ekindjian
DOI: 10.1186/AR1457
关键词: Endocrinology 、 Superoxide 、 Oxidative stress 、 Protein kinase C 、 In vitro 、 Tetradecanoylphorbol Acetate 、 Medicine 、 Internal medicine 、 Monocyte 、 In vivo 、 Nifedipine
摘要: We have reported previously that dihydropyridine-type calcium-channel antagonists (DTCCA) such as nifedipine decrease plasma markers of oxidative stress damage in systemic sclerosis (SSc). To clarify the cellular basis these beneficial effects, we investigated effects vivo and vitro on superoxide anion (O2•-) production by peripheral blood monocytes. compared 10 healthy controls with 12 patients SSc, first after interruption treatment DTCCA second 2 weeks (60 mg/day). O2•- monocytes stimulated phorbol myristate acetate (PMA) was quantified cytochrome c reduction method. also protein phosphorylation kinase C (PKC) activity using recombinant PKC. After had been washed out, from SSc produced more than those controls. Nifedipine considerably decreased PMA-stimulated Treatment inhibited PMA-induced a dose-dependent manner. Finally, strongly PKC vitro. Thus, observed is consistent overproduction primed This both property seems to be mediated its action inhibition activity. supports hypothesis this drug could useful for diseases associated stress.
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