J Nutr Health.  2017 Feb;50(1):25-31. 10.4163/jnh.2017.50.1.25.

Inhibitory effect of Petalonia binghamiae on neuroinflammation in LPS-stimulated microglial cells

• Park JH
• Kim SH
• Lee SR

• KMID: 2377978
• DOI: http://doi.org/10.4163/jnh.2017.50.1.25

Abstract

PURPOSE
Neuroinflammation is mediated by activation of microglia implicated in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. Inhibition of neuroinflammation may be an effective solution to treat these brain disorders. Petalonia binghamiae is known as a traditional food, based on multiple biological activities such as anti-oxidant and anti-obesity. In present study, the anti-neuroinflammatory potential of Petalonia binghamiae was investigated in LPS-stimulated BV2 microglial cells.
METHODS
Cell viability was measured by MTT assay. Production of nitric oxide (NO) was examined using Griess reagent. Expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) was detected by Western blot analysis. Activation of nuclear factor κB (NF-κB) signaling was examined by nuclear translocation of NF-κB p65 subunit and phosphorylation of IκB.
RESULTS
Extract of Petalonia binghamiae significantly inhibited LPS-stimulated NO production and iNOS/COX-2 protein expression in a dose-dependent manner without cytotoxicity. Pretreatment with Petalonia binghamiae suppressed LPS-induced NF-κB p65 nuclear translocation and phosphorylation of IκB. Co-treatment with Petalonia binghamiae and pyrrolidine duthiocarbamate (PDTC), an NF-κB inhibitor, reduced LPS-stimulated NO release compared to that in PB-treated or PDTC-treated cells.
CONCLUSION
The present results indicate that extract of Petalonia binghamiae exerts anti-neuroinflammation activities, partly through inhibition of NF-κB signaling. These findings suggest that Petalonia binghamiae might have therapeutic potential in relation to neuroinflammation and neurodegenerative diseases.

Keyword

Petalonia binghamiae; neuroinflammation; microglia; nitric oxide; nuclear factor-κB

MeSH Terms

Alzheimer Disease
Blotting, Western
Brain Diseases
Cell Survival
Cyclooxygenase 2
Microglia
Neurodegenerative Diseases
Nitric Oxide
Nitric Oxide Synthase
Parkinson Disease
Phosphorylation
Cyclooxygenase 2
Nitric Oxide
Nitric Oxide Synthase

Figure

• 

  Fig. 1. Effect of Petalonia binghamiae (PB) on the viability of BV-2 microglial cells. Cells were incubated with the indicated concentrations of PB for 24 h and cytotoxicity of PB was examined by MTT assay. Data are represented as mean ± SD of three independent experiments.

• 

  Fig. 2. Inhibitory effect of Petalonia binghamiae (PB) on LPS-induced NO production (A) and iNOS/COX-2 protein expression (B). The cells were incubated with the indicated concentrations of PB for 30 min before treatment of LPS. Data are represented as mean±SD of three independent experiments. Means with different letter in superscript are significantly different (p < 0.05) by ANOVA and Duncan's multiple range test.

• 

  Fig. 3. Effect of Petalonia binghamiae (PB) on the LPS-induced activation of NF-κB (p65) and IκB. The cells were treated with LPS (100 ng/mL) for 30 min in the absence and/or presence of PB (100 μg/mL). The cytoplasmic (C) and nuclear (N) extracts were prepared to determine translocation of NF-κB p65 and IκB activity was measured by levels of phosphorylated IκB protein.

• 

  Fig. 4. Involvement of NF-κB signaling on LPS-stimulated NO production. The cells were treated with LPS (100 ng/mL) for 24 h after treatment of PB (100 μg/mL) and/or PDTC (25 μM) for 30 min. Data are represented as mean ± SD of three independent experiments. Means sharing the same superscript letter are not are significantly different (p < 0.05) by ANOVA and Duncan's multiple range test.

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