Abstract
Inflammation is a defense mechanism that protects the body from infections. However, chronic inflammation causes damage to body tissues. Thus, controlling inflammation and investigating anti-inflammatory mechanisms are keys to preventing and treating inflammatory diseases, such as sepsis and rheumatoid arthritis. In continuation with our work related to the discovery of bioactive natural products, a polyphenol, catechin-7,4′-O-digallate (CDG), was isolated from Woodfordia uniflora, which has been used as a sedative and remedy for skin infections in the Dhofar region of Oman. Thus far, no study has reported the anti-inflammatory compounds derived from W. uniflora and the mechanisms underlying their action. To investigate the effects of CDG on the regulation of inflammation, we measured the reduction in nitric oxide (NO) production following CDG treatment in immortalized mouse Kupffer cells (ImKCs). CDG treatment inhibited NO production through the downregulation of inducible nitric oxide synthase expression in lipopolysaccharide (LPS)-stimulated ImKCs. The anti-inflammatory effects of CDG were mediated via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, an important inflammatory-response-associated signaling pathway. Moreover, CDG treatment has regulated the expression of pro-inflammatory cytokines, such as IL-6 and IL-1β. These results suggested the anti-inflammatory action of CDG in LPS-stimulated ImKCs.
Highlights
Based phenol extracted from green tea, known as epigallocatechin gallate, is a famous anti-inon the liquid chromatography/mass spectrometry (LC/MS)
Via Enzyme-Linked Immunosorbent Assay (ELISA), we demonstrated that the levels of IL-6 and IL-1β production were reduced by CDG treatment
We suggest that the inhibition of inducible nitric oxide synthase (iNOS) and IL-1β transcripof 12 tional activation by CDG treatment might be due to its selective regulatory effect on 9NFκB
Summary
Inflammation is a biological response to tissue damage or infection, and the main inflammatory mediators include immune cells, such as macrophages and neutrophils [1,2]. The purpose of inflammation is to suppress tissue damage and regenerate damaged cells. Chronic inflammation contributes to inflammatory diseases, such as inflammatory bowel disease, sepsis, and rheumatoid arthritis [3,4,5]. It is important to control the inflammation levels for the maintenance of homeostasis in the body. Inflammatory responses occur when immune cells in the body recognize infections and activate the inflammatory pathways, such as the nuclear factor kappa-light-chain-enhancer of Pharmaceutics 2021, 13, 408.
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