Journal List > J Nutr Health > v.50(1) > 1081500

J Nutr Health. 2017 Feb;50(1):25-31. Korean.
Published online February 28, 2017.
© 2017 The Korean Nutrition Society
Inhibitory effect of Petalonia binghamiae on neuroinflammation in LPS-stimulated microglial cells
Jae Hyeon Park, Sung Hun Kim and Sun Ryung Lee
Department of Biology, Jeju National University, Jeju 63243, Korea.

To whom correspondence should be addressed. tel: 82-64-754-3522, Email:
Received December 08, 2016; Revised December 20, 2016; Accepted January 18, 2017.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.



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.


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.


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.


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.

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


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.
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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.
Click for larger image

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.
Click for larger image

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.
Click for larger image


This work was supported by the project “PoINT” of Jeju National University in 2015.

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