Chrysin suppresses LPS-stimulated proinflammatory responses by blocking NF-κB and JNK activations in microglia cells

Neuroinflammation mediated by microglia has been implicated in neurodegenerative diseases. Suppression of microglial activation may therefore contribute to neuronal cell survival. Chrysin is present in honey and propolis and in low concentrations in fruits, vegetables, and certain beverages. It has been reported that chrysin has potent anti-inflammation, anti-cancer, and anti-oxidation properties. In the present study, we investigated the effects of chrysin on the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated microglia. Chrysin significantly inhibited the release of nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were also significantly inhibited by chrysin. Furthermore, chrysin inhibited the activations of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB), which are signaling molecules involved in neuroinflammation. These results suggest that chrysin may act as a potential therapeutic agent for various neurodegenerative diseases involving neuroinflammation.

Research highlights▶ Chrysin significantly decreased the productions of TNF-α and IL-1β in a dose-dependent manner in LPS-treated BV-2 cells. ▶ Chrysin also reduced the production of NF-κB and the phosphorylation of JNK. ▶ Inhibition of NF-κB and JNK activations by chrysin is responsible for the suppressions of iNOS and COX-2. ▶ Chrysin inhibited the LPS-induced increases in NO in BV-2 cells.