Punicalagin inhibits neuroinflammation in LPS-activated rat primary microglia

Olumayokun A. Olajide, Asit Kumar, Ravikanth Velagapudi, Uchechukwu P. Okorji, Bernd L. Fiebich

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31 Citations (Scopus)

Abstract

Scope: In this study, the effects of punicalagin on neuroinflammation in LPS-activated microglia were investigated. Methods and results: The ability of punicalagin to reduce the production of TNF-α, IL-6 and prostaglandin E2 was measured in culture medium using enzyme immunoassay. TNF-α and IL-6 gene expression in mouse hippocampal slices was measured with PCR. cyclooxygenase-2 and microsomal prostaglandin E synthase 1 protein and mRNA were evaluated with Western blotting and PCR, respectively. Further experiments to investigate effects of punicalagin on protein expressions of inflammatory targets were also determined with Western blotting. Pretreatment of rat primary microglia with punicalagin (5-40 μM) prior to LPS (10 ng/mL) stimulation produced a significant (p < 0.05) inhibition of TNF-α, IL-6 and prostaglandin E2 production. Punicalagin completely abolished TNF-α and IL-6 gene expression in LPS-stimulated hippocampal slices. Protein and mRNA expressions of cyclooxygenase-2 and microsomal prostaglandin E synthase 1 were also reduced by punicalagin pretreatment. Results show that punicalagin interferes with NF-κB signalling through attenuation of NF-κB-driven luciferase expression, as well as inhibition of IκB phosphorylation and nuclear translocation of p65 subunit in the microglia. Conclusion: These results suggest that punicalagin inhibits neuroinflammation in LPS-activated microglia through interference with NF-κB signalling, suggesting its potential as a nutritional preventive strategy in neurodegenerative disorders. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
LanguageEnglish
Pages1843-1851
JournalMolecular Nutrition and Food Research
Volume58
Issue number9
DOIs
Publication statusPublished - 1 Sep 2014

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neuroglia
Microglia
interleukin-6
tumor necrosis factor-alpha
rats
prostaglandin synthase
prostaglandins
Interleukin-6
Western blotting
pretreatment
Tumor Necrosis Factor-alpha
gene expression
enzyme immunoassays
neurodegenerative diseases
Cyclooxygenase 2
luciferase
crossover interference
Dinoprostone
phosphorylation
proteins

Cite this

Olajide, Olumayokun A. ; Kumar, Asit ; Velagapudi, Ravikanth ; Okorji, Uchechukwu P. ; Fiebich, Bernd L. / Punicalagin inhibits neuroinflammation in LPS-activated rat primary microglia. In: Molecular Nutrition and Food Research. 2014 ; Vol. 58, No. 9. pp. 1843-1851.
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Punicalagin inhibits neuroinflammation in LPS-activated rat primary microglia. / Olajide, Olumayokun A.; Kumar, Asit; Velagapudi, Ravikanth; Okorji, Uchechukwu P.; Fiebich, Bernd L.

In: Molecular Nutrition and Food Research, Vol. 58, No. 9, 01.09.2014, p. 1843-1851.

Research output: Contribution to journalArticle

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T1 - Punicalagin inhibits neuroinflammation in LPS-activated rat primary microglia

AU - Olajide, Olumayokun A.

AU - Kumar, Asit

AU - Velagapudi, Ravikanth

AU - Okorji, Uchechukwu P.

AU - Fiebich, Bernd L.

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N2 - Scope: In this study, the effects of punicalagin on neuroinflammation in LPS-activated microglia were investigated. Methods and results: The ability of punicalagin to reduce the production of TNF-α, IL-6 and prostaglandin E2 was measured in culture medium using enzyme immunoassay. TNF-α and IL-6 gene expression in mouse hippocampal slices was measured with PCR. cyclooxygenase-2 and microsomal prostaglandin E synthase 1 protein and mRNA were evaluated with Western blotting and PCR, respectively. Further experiments to investigate effects of punicalagin on protein expressions of inflammatory targets were also determined with Western blotting. Pretreatment of rat primary microglia with punicalagin (5-40 μM) prior to LPS (10 ng/mL) stimulation produced a significant (p < 0.05) inhibition of TNF-α, IL-6 and prostaglandin E2 production. Punicalagin completely abolished TNF-α and IL-6 gene expression in LPS-stimulated hippocampal slices. Protein and mRNA expressions of cyclooxygenase-2 and microsomal prostaglandin E synthase 1 were also reduced by punicalagin pretreatment. Results show that punicalagin interferes with NF-κB signalling through attenuation of NF-κB-driven luciferase expression, as well as inhibition of IκB phosphorylation and nuclear translocation of p65 subunit in the microglia. Conclusion: These results suggest that punicalagin inhibits neuroinflammation in LPS-activated microglia through interference with NF-κB signalling, suggesting its potential as a nutritional preventive strategy in neurodegenerative disorders. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

AB - Scope: In this study, the effects of punicalagin on neuroinflammation in LPS-activated microglia were investigated. Methods and results: The ability of punicalagin to reduce the production of TNF-α, IL-6 and prostaglandin E2 was measured in culture medium using enzyme immunoassay. TNF-α and IL-6 gene expression in mouse hippocampal slices was measured with PCR. cyclooxygenase-2 and microsomal prostaglandin E synthase 1 protein and mRNA were evaluated with Western blotting and PCR, respectively. Further experiments to investigate effects of punicalagin on protein expressions of inflammatory targets were also determined with Western blotting. Pretreatment of rat primary microglia with punicalagin (5-40 μM) prior to LPS (10 ng/mL) stimulation produced a significant (p < 0.05) inhibition of TNF-α, IL-6 and prostaglandin E2 production. Punicalagin completely abolished TNF-α and IL-6 gene expression in LPS-stimulated hippocampal slices. Protein and mRNA expressions of cyclooxygenase-2 and microsomal prostaglandin E synthase 1 were also reduced by punicalagin pretreatment. Results show that punicalagin interferes with NF-κB signalling through attenuation of NF-κB-driven luciferase expression, as well as inhibition of IκB phosphorylation and nuclear translocation of p65 subunit in the microglia. Conclusion: These results suggest that punicalagin inhibits neuroinflammation in LPS-activated microglia through interference with NF-κB signalling, suggesting its potential as a nutritional preventive strategy in neurodegenerative disorders. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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