Abstract
The brain is sensitive to the inflammation and oxidative stress that can cause the aging or neurodegenerative diseases. We investigated the anti-neuroinflammatory activities of taurine chloramine (TauCl) on lipopolysaccharide (LPS)-treated mouse BV2 microglia mediated through heme oxygenase (HO)-1 expression. TauCl inhibited the protein expressions of prostaglandin E2 (PGE2), cyclooxygenase (COX)-2, nitric oxide (NO), and inducible nitric oxide synthase (iNOS) in LPS-treated BV2 microglia. TauCl markedly inhibited interleukin-6 (IL-6), interleukin-1𝛽 (IL-1𝛽) and tumor necrosis factor-𝛼 (TNF-𝛼) production. These effects were related to the suppression of the degradation and phosphorylation of inhibition of nuclear factor kappa B-𝛼 (I𝜅B-𝛼), translocation of nuclear factor kappa B (NF-𝜅B) as well as DNA binding activity. In addition, TauCl induced the HO-1 expression by increasing the nuclear factor E2-related factor 2 (Nrf2) translocation to the nucleus in mouse BV2 microglia. These findings suggest that TauCl has protective effects of neurodegenerative disorders caused by neuroinflammation.
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Abbreviations
- (IκB)-α:
-
Inhibitor kappa B-α
- COX-2:
-
Cyclooxygenase-2
- HO:
-
Heme oxygenase
- IL-1β:
-
Interleukin-1β
- IL-6:
-
Interleukin-6
- iNOS:
-
Inducible nitric oxide synthase
- LPS:
-
Lipopolysaccharide
- NF-κB:
-
Nuclear factor-kappa B
- NO:
-
Nitric oxide
- Nrf2:
-
Nuclear factor-E2-related factor 2
- PGE2 :
-
Prostaglandin E2
- TauCl:
-
Taurine chloramine
- TNF-α:
-
Necrosis factor-α
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Acknowledgements
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2016R1D1A1B01006822).
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Lee, DS., Kwon, K.H., Cheong, S.H. (2017). Taurine Chloramine Suppresses LPS-Induced Neuroinflammatory Responses through Nrf2-Mediated Heme Oxygenase-1 Expression in Mouse BV2 Microglial Cells. In: Lee, DH., Schaffer, S.W., Park, E., Kim, H.W. (eds) Taurine 10. Advances in Experimental Medicine and Biology, vol 975. Springer, Dordrecht. https://doi.org/10.1007/978-94-024-1079-2_12
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DOI: https://doi.org/10.1007/978-94-024-1079-2_12
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