In vitro and in vivo inhibitory effects of 6-hydroxyrubiadin on lipopolysaccharide-induced inflammation.

Inflammation is a defensive response against a multitude of harmful stimuli and stress conditions such as tissue injury, and is one of the most common pathological processes of human diseases. 6-Hydroxyrubiadin, an anthraquinone isolated from Rubia cordifolia L., exhibits several bioactive properties. The aim of this study was to evaluate whether 6-hydroxyrubiadin can reduce the production of pro-inflammatory cytokines and ameliorate acute lung injury (ALI) in a mouse model. In this study, we demonstrated that 6-hydroxyrubiadin suppressed lipopolysaccharide (LPS)-induced nuclear factor-kappa B activation as well as the phosphorylation of c-Jun N-terminal kinase in RAW 264.7 macrophages. In addition, we also showed that 6-hydroxyrubiadin inhibited the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in phorbol myristate acetate (PMA)-primed U937 and RAW 264.7 cells. Furthermore, 6-hydroxyrubiadin treatment reduced the production of these cytokines in vivo and attenuated the severity of LPS-induced ALI. Thus, these results suggested that 6-hydroxyrubiadin may be a potential therapeutic candidate for the treatment of inflammation and inflammatory diseases.