Benfotiamine upregulates antioxidative system in activated BV-2 microglia cells
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Published on: October 25, 2016
Iva Bozic1, Danijela Savic1, Ivana Stevanovic2
1Institute for Biological Research "Siniša Stanković," University of Belgrade Belgrade, Serbia.
Abstract:
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 O-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(-) 2 production and lipid peroxidation. In conclusion, benfotiamine might silence pro-oxidative activity of microglia to alleviate/prevent oxidative damage of neighboring CNS cells.
Insights
Benfotiamine reduces oxidative stress in activated microglia, a key factor in neurodegeneration. This vitamin B1 derivative enhances antioxidant defenses and scavenges harmful radicals, protecting neurons from damage.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Chronic microglial activation drives neuroinflammation and neurodegeneration.
- Activated microglia produce cytotoxic mediators like superoxide and nitric oxide.
- Benfotiamine has demonstrated anti-inflammatory properties.
Purpose of the Study:
- To investigate the effects of benfotiamine on the pro-oxidative activity of lipopolysaccharide (LPS)-stimulated microglia.
- To determine if benfotiamine can modulate the antioxidant defense system in activated microglia.
Main Methods:
- Utilized LPS-stimulated BV-2 microglial cells.
- Assessed intracellular antioxidant enzyme levels and activities (catalase, glutathione system, superoxide dismutase).
- Measured direct scavenging of superoxide radical anion by benfotiamine.
- Quantified nitric oxide and superoxide production, and lipid peroxidation.
Main Results:
- Benfotiamine upregulated intracellular antioxidant defenses in activated microglia.
- Increased levels and activities of catalase, glutathione system, and superoxide dismutase were observed.
- Benfotiamine directly scavenged superoxide radical anions.
- Suppressed microglial activation, reducing nitric oxide, superoxide production, and lipid peroxidation.
Conclusions:
- Benfotiamine effectively silences the pro-oxidative activity of microglia.
- It enhances endogenous antioxidant systems and directly neutralizes reactive oxygen species.
- Benfotiamine shows potential in alleviating or preventing oxidative damage to central nervous system (CNS) cells.
