The effects of malvidin on oxidative stress parameters and inflammatory cytokines in LPS‐induced human THP‐1 cells

Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. THP‐1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study ai...

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Veröffentlicht in:Journal of cellular physiology 2021-04, Vol.236 (4), p.2790-2799
Hauptverfasser: Bastin, Alireza, Sadeghi, Asie, Nematollahi, Mohammad Hadi, Abolhassani, Moslem, Mohammadi, Abbas, Akbari, Hamed
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container_issue 4
container_start_page 2790
container_title Journal of cellular physiology
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creator Bastin, Alireza
Sadeghi, Asie
Nematollahi, Mohammad Hadi
Abolhassani, Moslem
Mohammadi, Abbas
Akbari, Hamed
description Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. THP‐1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study aimed to investigate the effect of malvidin on inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced THP‐1 cells. THP‐1 cells were stimulated with LPS (50 ng/ml) to induce inflammation in the presence or absence of malvidin. The anti/proinflammatory cytokines were evaluated by real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay. Total protein levels/phosphorylation of c‐Jun N‐terminal kinase (JNK), P65‐NF‐κB, and IKKα/IKKβ were evaluated by western blot analysis. Malondialdehyde (MDA) and nitric oxide (NO) metabolite levels, ferric reducing antioxidant power (FRAP), total thiol (T‐SH) content, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured to evaluate the antioxidant activity of malvidin in THP‐1 cells. Treatment of LPS‐stimulated THP‐1 cells with malvidin (100 and 200 μM) led to the significant inhibition of interleukin‐6 (IL‐6), tumor necrosis factor‐α, and IL‐1β messenger RNA (mRNA) expression and protein levels as well as a significant increase in the IL‐10 mRNA expression and protein secretion. Moreover, 200 μM malvidin treatment reduced the phosphorylation of JNK, IKKα/IKKβ, and P65‐NF‐κB. These findings showed that malvidin not only decreased the MDA and NO metabolite levels but also increased the FRAP and T‐SH content as well as SOD and GPx activities. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by LPS in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases. Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by lipopolysaccharide in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases.
doi_str_mv 10.1002/jcp.30049
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THP‐1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study aimed to investigate the effect of malvidin on inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced THP‐1 cells. THP‐1 cells were stimulated with LPS (50 ng/ml) to induce inflammation in the presence or absence of malvidin. The anti/proinflammatory cytokines were evaluated by real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay. Total protein levels/phosphorylation of c‐Jun N‐terminal kinase (JNK), P65‐NF‐κB, and IKKα/IKKβ were evaluated by western blot analysis. Malondialdehyde (MDA) and nitric oxide (NO) metabolite levels, ferric reducing antioxidant power (FRAP), total thiol (T‐SH) content, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured to evaluate the antioxidant activity of malvidin in THP‐1 cells. Treatment of LPS‐stimulated THP‐1 cells with malvidin (100 and 200 μM) led to the significant inhibition of interleukin‐6 (IL‐6), tumor necrosis factor‐α, and IL‐1β messenger RNA (mRNA) expression and protein levels as well as a significant increase in the IL‐10 mRNA expression and protein secretion. Moreover, 200 μM malvidin treatment reduced the phosphorylation of JNK, IKKα/IKKβ, and P65‐NF‐κB. These findings showed that malvidin not only decreased the MDA and NO metabolite levels but also increased the FRAP and T‐SH content as well as SOD and GPx activities. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by LPS in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases. Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. 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THP‐1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study aimed to investigate the effect of malvidin on inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced THP‐1 cells. THP‐1 cells were stimulated with LPS (50 ng/ml) to induce inflammation in the presence or absence of malvidin. The anti/proinflammatory cytokines were evaluated by real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay. Total protein levels/phosphorylation of c‐Jun N‐terminal kinase (JNK), P65‐NF‐κB, and IKKα/IKKβ were evaluated by western blot analysis. Malondialdehyde (MDA) and nitric oxide (NO) metabolite levels, ferric reducing antioxidant power (FRAP), total thiol (T‐SH) content, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured to evaluate the antioxidant activity of malvidin in THP‐1 cells. Treatment of LPS‐stimulated THP‐1 cells with malvidin (100 and 200 μM) led to the significant inhibition of interleukin‐6 (IL‐6), tumor necrosis factor‐α, and IL‐1β messenger RNA (mRNA) expression and protein levels as well as a significant increase in the IL‐10 mRNA expression and protein secretion. Moreover, 200 μM malvidin treatment reduced the phosphorylation of JNK, IKKα/IKKβ, and P65‐NF‐κB. These findings showed that malvidin not only decreased the MDA and NO metabolite levels but also increased the FRAP and T‐SH content as well as SOD and GPx activities. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by LPS in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases. Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. 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however, its mechanism of action in THP‐1 cells is not yet known. THP‐1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study aimed to investigate the effect of malvidin on inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced THP‐1 cells. THP‐1 cells were stimulated with LPS (50 ng/ml) to induce inflammation in the presence or absence of malvidin. The anti/proinflammatory cytokines were evaluated by real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay. Total protein levels/phosphorylation of c‐Jun N‐terminal kinase (JNK), P65‐NF‐κB, and IKKα/IKKβ were evaluated by western blot analysis. Malondialdehyde (MDA) and nitric oxide (NO) metabolite levels, ferric reducing antioxidant power (FRAP), total thiol (T‐SH) content, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured to evaluate the antioxidant activity of malvidin in THP‐1 cells. Treatment of LPS‐stimulated THP‐1 cells with malvidin (100 and 200 μM) led to the significant inhibition of interleukin‐6 (IL‐6), tumor necrosis factor‐α, and IL‐1β messenger RNA (mRNA) expression and protein levels as well as a significant increase in the IL‐10 mRNA expression and protein secretion. Moreover, 200 μM malvidin treatment reduced the phosphorylation of JNK, IKKα/IKKβ, and P65‐NF‐κB. These findings showed that malvidin not only decreased the MDA and NO metabolite levels but also increased the FRAP and T‐SH content as well as SOD and GPx activities. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by LPS in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases. Malvidin is an anthocyanin which is involved in inhibiting inflammatory‐related mediators in inflammatory diseases; however, its mechanism of action in THP‐1 cells is not yet known. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by lipopolysaccharide in THP‐1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32914418</pmid><doi>10.1002/jcp.30049</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5241-9856</orcidid><orcidid>https://orcid.org/0000-0002-9529-4077</orcidid></addata></record>
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subjects Acute monocytic leukemia
Anthocyanins
Antioxidants
Biotechnology
Chemical compounds
Cytokines
Evaluation
Gene expression
Glutathione
Glutathione peroxidase
inflammation
Inflammatory diseases
Interleukins
JNK protein
Kinases
Leukemia
Lipopolysaccharides
Malondialdehyde
malvidin
Metabolites
Monocytes
Monocytic leukemia
Nitric oxide
Oxidative stress
Peroxidase
Pharmacology
Phosphorylation
Polymerase chain reaction
Proteins
Superoxide dismutase
THP‐1 cells
title The effects of malvidin on oxidative stress parameters and inflammatory cytokines in LPS‐induced human THP‐1 cells
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