Selenium-enriched oolong tea (Camellia sinensis) extract exerts anti-inflammatory potential via targeting NF-κB and MAPK pathways in macrophages

Both tea polyphenols and selenium (Se) have been suggested to exert the health benefits via the regulatory capacities of chronic inflammation, which make Se-enriched oolong tea a promising beverage as an anti-inflammatory diet. The aim of this study is to investigate the anti-inflammatory effects of Se-enriched oolong tea extract (Se-TE) and underlying mechanism in lipopolysaccharide (LPS)-induced RAW264.7 cells. Se-TE treatments (50 and 150 mu g/mL) significantly suppressed the over-production of nitric oxide (NO) and prostaglandin E2 (PGE(2)) in LPS-stimulated macrophages via downregulating the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Moreover, Se-TEs also effectively inhibited the productions of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta). Furthermore, Se-TE could block mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) signaling pathways through the inhibition of the phosphorylation of key proteins (I kappa B-alpha, p65, p38, ERK, and JNK) and the translocation of the p65 subunit into the nucleus. Collectively, our results indicated that Se-TE may have the potential to be used as a novel food ingredient for the development of various anti-inflammatory foods and the treatment and prevention of chronic inflammation-related diseases. (C) 2022 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

Automated summary

The study investigated the anti-inflammatory effects of selenium-enriched oolong tea extract (Se-TE) on lipopolysaccharide-induced macrophages. The results showed that Se-TE significantly suppressed the overproduction of nitric oxide and prostaglandin E2, as well as inhibited the production of inflammatory cytokines. The underlying mechanism involved the blocking of mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.