Prophylactic effect of Biochanin A in lipopolysaccharide-stimulated BV2 microglial cells

Abstract

Aim/Purpose of the study:Inhibition of microglial activation using phytochemicals may be a potential candidate for the prevention of neurodegenerative diseases caused by neuroinflammation and oxidative stress. The goal of this study was to investigate the protective role of Biochanin A on lipopolysaccharide (LPS)-stimulated BV2 microglial cells. BV2 microglial cells were treated with LPS in the presence and absence of Biochanin A. Materials and methods: For this aim, nitric oxide production, nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, Prostaglandin E2 (PGE2), and reactive oxygen species (ROS) levels, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), myeloid differentiation factor-88 (MyD88), and toll like receptor-4 (TLR-4) protein expressions, Akt and ERK1/2 phosphorylation levels were measured. Results:Biochanin A pretreatment resulted in significant and concentration-dependently reduced the LPS-induced production of nitric oxide, NF-κB p65, TNF-α, IL-1β, IL-6, PGE2, and ROS compared to the untreated group. Biochanin A prophylaxis exerted an anti-inflammatory effect by suppressing iNOS, COX-2, MyD88, and TLR-4 protein expressions and Akt and ERK1/2 pathway activation. Conclusion:Taken together, these results show that Biochanin A exerts antioxidant and anti-inflammatory activities, thus may be beneficial for preventing neurodegenerative diseases mediated by microglial cells.

Keywords:

• Biochanin A
• BV2 microglial cells
• neuroinflammation
• nuclear factor kappa B
• reactive-oxygen species

Acknowledgement

The authors would like to thank Mr. Alexander B. Hunt for English language editing of the manuscript.

Disclosure statement

No conflict of interest was declared by the author(s).

Additional information

Funding

This research was financially supported in part by the Office of Scientific Research Projects of Mersin University under Grant number [2016-2-TP3-1891].