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

• Published in: Immunopharmacology and immunotoxicology Vol. 42; no. 4; pp. 330 - 339
• Main Authors: Berköz, Mehmet, Krośniak, Mirosław, Özkan-Yılmaz, Ferbal, Özlüer-Hunt, Arzu
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 15.07.2020
• Subjects: Animals; Anticarcinogenic Agents - administration & dosage; Biochanin A; BV2 microglial cells; Cell Line; Cell Survival - drug effects; Cell Survival - physiology; Dose-Response Relationship, Drug; Genistein - administration & dosage; Lipopolysaccharides - toxicity; Mice; Microglia - drug effects; Microglia - metabolism; neuroinflammation; nuclear factor kappa B; Pre-Exposure Prophylaxis - methods; Reactive Oxygen Species - antagonists & inhibitors; Reactive Oxygen Species - metabolism; reactive-oxygen species; reactive-oxygen species; Biochanin A; neuroinflammation; BV2 microglial cells; nuclear factor kappa B
• ISSN: 0892-3973; 1532-2513
• DOI: 10.1080/08923973.2020.1769128

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.