Benfotiamine upregulates antioxidative system in activated BV-2 microglia cells
2015
Аутори:
Božić, IvaSavić, Danijela
Stevanovic, Ivana
Peković, Sanja
Nedeljkovic, Nadezda
Lavrnja, Irena
Тип документа:
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт:
Chronic microglial activation and resulting sustained neuroinflammatory
reaction are generally associated with neurodegeneration. Activated
microglia acquires proinflammatory cellular profile that generates
oxidative burst. Their persistent activation exacerbates inflammation,
which damages healthy neurons via cytotoxic mediators, such as
superoxide radical anion and nitric oxide. In our recent study, we have
shown that benfotiamine (S-benzoylthiamine 0-monophosphate) possesses
anti-inflammatory effects. Here, the effects of benfotiamine on the
pro-oxidative component of activity of LPS-stimulated BV -2 cells were
investigated. The activation of microglia was accompanied by
upregulation of intracellular antioxidative defense, which was further
promoted in the presence of benfotiamine. Namely, activated microglia
exposed to non-cytotoxic doses of benfotiamine showed increased levels
and activities of hydrogen peroxide- and superoxide removing enzymes
catalase and glutathione system, and superoxide dismutase. In addition,
benfotiamine showed the capacity to directly scavenge superoxide radical
anion. As a consequence, benfotiamine suppressed the activation of
microglia and provoked a decrease in NO and O-center dot(2)- production
and lipid peroxidation. In conclusion, benfotiamine might silence
pro-oxidative activity of microglia to alleviate/prevent oxidative
damage of neighboring CNS cells.
Кључне речи:
benfotiamine; microglia; oxidative stress; catalase; glutathioneИзвор:
Frontiers in Cellular Neuroscience, 2015, 9, 351
DOI: 10.3389/fncel.2015.00351
ISSN: 1662-5102