Benfotiamine upregulates antioxidative system in activated BV-2 microglia cells

Božić, Iva; Savić, Danijela; Stevanović, Ivana; Peković, Sanja; Nedeljković, Nadežda; Lavrnja, Irena

doi:10.3389/fncel.2015.00351

Cited by 30 publications

(34 citation statements)

References 75 publications

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“…However, the diets were isocaloric with few differences between activity was higher than non-supplemented groups, suggesting that SOD activity in gastrocnemius muscle was increased in response to benfotiamine supplementation. This data shows the effect of benfotiamine on SOD efficiency, in agreement with other studies that showed positive effects of thiamine analogous in SOD activity and gene expression (Bozic et al, 2015;Vidhya, Renjugopal & Indira 2013). In addition, the results of this study suggest that there was a combined effect of exercise and benfotiamine supplementation, since the Ben-Sed group did not show an increase in SOD activity, unlike the Ben-Tr.…”

Section: Discussionsupporting

confidence: 92%

“…Some experimental studies have demonstrated the antioxidant capacity of thiamine (vitamin B1) (Gioda et al, 2010;Karachalias, Babaei-Jadidi, Rabbani, & Thornalley, 2010;Portari, Ovidio, Deminice & Jordão Jr, 2016). Aside from thiamine being efficient in transferring ions to the reactive species (Lukienko, Mel'nichenko, Zverinskii & Zabrodskaya, 2000), there are evidences that the treatment with benfotiamine, a lipophilic thiamine derivate, increased protein expression and activity of antioxidant enzymes in culture of neurological cells (Bozic et al, 2015). Thiamine diphosphate is an essential coenzyme in the pentose phosphate pathway, which produces reduced nicotinamide adenine dinucleotide phosphate (NADPH), a molecule which transfer their Hto highly reactive molecules and is essential for the activity of the antioxidant enzymes catalase (CAT) and glutathione peroxidase (GPx) (Stincone et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Benfotiamine reduces oxidative damage in muscle of endurance-trained mouse.

Gonçalves

Leao

Orsatti

et al. 2019

Acta Sci. Health Sci.

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High levels of reactive oxygen species can trigger an imbalance in redox status, which generates oxidative damage in macromolecules. The present study aimed to investigate the influence of oral supplementation with benfotiamine on oxidative stress and antioxidant activity in muscle of trained mice. Twenty-five male Balb/c mice were placed in groups. Sta-Sed: standard diet and sedentary (n = 6); Ben-Sed: benfotiamine supplemented and sedentary (n = 6); Sta-Tr: standard diet and trained (n = 6); and Ben-Tr: benfotiamine supplemented and trained (n = 7). Standard diet was AIN-93 growth and supplemented diet was AIN-93 with benfotiamine (500 mg kg -1 ). Trained mice were submitted to 6-weeks of endurance swimming training. The concentration of thiobarbituric acid reactive substances (TBARS), non-protein thiols, catalase (CAT) and superoxide dismutase activities (SOD) were analyzed in the gastrocnemius muscle. TBARS concentration was lower in the Ben-Tr group than in Ben-Sed and Sta-Tr groups. Thiol levels were higher in the Ben-Sed group than in the non-supplemented groups. CAT activity was more pronounced in both supplemented groups while SOD activity was higher in the Ben-Tr group than in the non-supplemented groups. The results show that benfotiamine supplementation is effective in enhancing antioxidant defenses and reducing oxidative damage in muscle of endurance-trained mouse.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Benfotiamine reduces oxidative damage in muscle of endurance-trained mouse.

Gonçalves

Leao

Orsatti

et al. 2019

Acta Sci. Health Sci.

View full text Add to dashboard Cite

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“…These two populations of cells are functionally distinct; however, it is postulated that both macrophages and microglia have a role in EAE pathogenesis (Duffy, Lees, & Moalem-Taylor, 2014 (Lampron et al, 2015). Activated microglia display a proinflammatory phenotype that leads to a "vicious cycle of inflammation" (Kettenmann, Hanisch, Noda, & Verkhratsky, 2011), which is characterized by production of potentially neurotoxic substances, such as proinflammatory cytokines and oxygen/nitrogen radicals (Bozic, Savic, Stevanovic, et al, 2015;Hanisch, 2013). Activated microglia may induce reactive astrocytes to be neurotoxic .…”

Section: Histopathology Of Eaementioning

confidence: 99%

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Bjelobaba

Begović-Kuprešanin

Peković

et al. 2018

J of Neuroscience Research

Self Cite

137

102

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Multiple sclerosis (MS) is a chronic, progressive disorder of the central nervous system (CNS) that affects more than two million people worldwide. Several animal models resemble MS pathology; the most employed are experimental autoimmune encephalomyelitis (EAE) and toxin- and/or virus-induced demyelination. In this review we will summarize our knowledge on the utility of different animal models in MS research. Although animal models cannot replicate the complexity and heterogeneity of the MS pathology, they have proved to be useful for the development of several drugs approved for treatment of MS patients. This review focuses on EAE because it represents both clinical and pathological features of MS. During the past decades, EAE has been effective in illuminating various pathological processes that occur during MS, including inflammation, CNS penetration, demyelination, axonopathy, and neuron loss mediated by immune cells.

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“…This combination produces the powerful pro-oxidant peroxynitrite (ONOO − ) which can cause neurotoxic injury to surrounding neurons and thereby contribute to the progressive damage observed in neurodegenerative diseases (ND) [11, 12, 15–24]. Microglia-derived excessive oxidative stress and chronic neuroinflammation have more recently been recognized as important pathological events in Alzheimer’s disease (AD), especially in the onset and development of the disease [25–30]. …”

Section: Introductionmentioning

confidence: 99%

The Antioxidant Effects of Thymoquinone in Activated BV-2 Murine Microglial Cells

et al. 2016

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Both neuroinflammation and microglial activation are pathological markers of a number of central nervous system (CNS) diseases. During chronic activation of the microglial cells, the induced release of excessive amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines have been implicated in several neurodegenerative diseases such as Alzheimer’s disease. Thymoquinone (TQ), a major bioactive compound of the natural product Nigella sativa seed, has been shown to be effective against numerous oxidative stress-induced and inflammatory disorders as well as possess neuroprotective properties. In this study, we investigated the antioxidant effects of TQ on LPS/IFNγ or H2O2-activated BV-2 microglia by assessing the levels of specific oxidative stress markers, the activities of selected antioxidant enzymes, as well as profiling 84 key genes related to oxidative stress via real-time reverse transcription (RT2) PCR array. Our results showed that in the LPS/IFNγ-activated microglia TQ significantly decreased the cellular production of both superoxide and nitric oxide 4-fold (p<0.0001) and 6 fold (p<0.0001), respectfully. In the H2O2-activated microglia, TQ also significantly decreased the cellular production of superoxide 3-fold (p<0.0001) and significantly decreased hydrogen peroxide levels ~20% (p<0.05). Moreover, TQ treatment significantly decreased the levels oxidative stress in the activated BV-2 as evidenced by the assessed levels of lipid hydroperoxides and glutathione. TQ significantly decreased the levels of lipid hydroperoxides 2-fold (p<0.0001) and significantly increased the levels of antioxidant glutathione 2.5-fold (p<0.0001) in the LPS/IFNγ-activated BV-2 cells. In the H2O2-activated microglia, TQ significantly decreased lipid hydroperoxides 8-fold (p<0.0001) and significantly increased glutathione 15% (p<0.05). Activities of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), in the TQ-treated microglial cells also reflected a reduced oxidative stress status in the cellular environment. SOD and CAT activities were 6 fold (p<0.0001) and 5 fold (p<0.0001) lower, respectfully, for the LPS/INFγ-activated microglia treated with TQ in comparison to those that were not. For the H2O2-activated microglia treated with TQ, SOD and CAT activities were 5 fold (p<0.0001) and 3 fold (p<0.01) lower, respectfully, compared to the untreated. Furthermore, RT2 PCR array profiling of the selected 84 genes related to oxidative stress confirmed that TQ treatment in the LPS/IFNγ-activated microglia downregulates specific pro-oxidant genes, upregulates specific anti-oxidant genes, and enhances the up- or downregulation of specific genes related to the cells’ natural antioxidant defense against LPS/IFNγ activation. These findings suggest that TQ may be utilized as an effective therapeutic agent for delaying the onset and/or slowing/preventing the progression of microglia-derived neurodegeneration propagated by excessive oxidative stress in the CNS.

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Benfotiamine upregulates antioxidative system in activated BV-2 microglia cells

Cited by 30 publications

References 75 publications

Benfotiamine reduces oxidative damage in muscle of endurance-trained mouse.

Benfotiamine reduces oxidative damage in muscle of endurance-trained mouse.

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

The Antioxidant Effects of Thymoquinone in Activated BV-2 Murine Microglial Cells

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