Abstract
Biorenovation is a microbial enzyme-catalyzed structural modification of organic compounds with the potential benefits of reduced toxicity and improved biological properties relative to their precursor compounds. In this study, we synthesized a novel compound verified as formononetin 7-O-phosphate (FMP) from formononetin (FM) using microbial biotransformation. We further compared the anti-inflammatory properties of FMP to FM in lipopolysaccharide (LPS)-treated RAW264.7 macrophage cells. We observed that cell viabilities and inhibitory effects on LPS-induced nitric oxide (NO) production were greater in FMP-treated RAW 264.7 cells than in their FM-treated counterparts. In addition, FMP treatment suppressed the production of proinflammatory cytokines such as prostaglandin-E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in a dose-dependent manner and concomitantly decreased the mRNA expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). We also found that FMP exerted its anti-inflammatory effects through the downregulation of the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor kappa B (NF-κB) signaling pathways. In conclusion, we generated a novel anti-inflammatory compound using biorenovation and demonstrated its efficacy in cell-based in vitro assays.
Highlights
Inflammation is an early host immune reaction mediated by cytokines secreted from immune cells [1,2]
Bacillus amyloliquefaciens KCTC 13,588 was used for the production of biorenovation derivatives of FM
Electrospray ionization–mass spectrometry (ESI/MS) analysis was performed to determine if the compound was a derivative of FM
Summary
Inflammation is an early host immune reaction mediated by cytokines secreted from immune cells [1,2] This response plays a key role in the development of various human chronic diseases, including bronchitis, cancer, diabetes, and rheumatoid arthritis [3]. Macrophages are activated by stimuli such as interferon-γ (IFN-γ), bacterial lipopolysaccharides (LPS), proinflammatory cytokines (including tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)), extracellular matrix proteins, and other chemical mediators [5]. Upon activation by these stimuli, macrophages produce numerous proinflammatory mediators, such as nitric oxide (NO), prostaglandin-E2 (PGE2), and TNF-α, to promote inflammatory responses [6]. NO is a key signaling molecule in a number of biological processes, including vasodilation, Molecules 2019, 24, 3910; doi:10.3390/molecules24213910 www.mdpi.com/journal/molecules
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