Anti-inflammatory effect of the extracts from the branch of Taxillus yadoriki being parasitic in Neolitsea sericea in LPS-stimulated RAW264.7 cells

• Published in: Biomedicine & pharmacotherapy Vol. 104; pp. 1 - 7
• Main Authors: Park, Su Bin, Park, Gwang Hun, Kim, Ha Na, Son, Ho-Jun, Song, Hun Min, Kim, Hyun-Seok, Jeong, Hyung Jin, Jeong, Jin Boo
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.08.2018
• Subjects: Anti-inflammation; Inflammatory response; Mistletoe; Taxillus yadoriki; Inflammatory response; Taxillus yadoriki; Mistletoe; Anti-inflammation
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.05.034

[Display omitted] •TY-NS-B blocks NO and PGE2 production by inhibiting iNOS and COX-2 expression.•TY-NS-B attenuates TNF-α and IL-1β expression.•TY-NS-B inhibits NF-κB activating by inhibiting IκB-α degradation and subsequent p65 nucleus translocation.•TY-NS-B inhibits p38 and JNK activation.•TY-NS-B activates ATF3 expression. Mistletoe has been used as the herbal medicine to treat hypertension, diabetes mellitus, inflammation, arthritis and viral infection. In this study, we evaluated the anti-inflammatory effect of extracts of branch from Taxillus yadoriki being parasitic in Neolitsea sericea (TY-NS-B) using in vitro model. TY-NS-B significantly inhibited LPS-induced secretion of NO and PGE2 in RAW264.7 cells. TY-NS-B was also observed to inhibit LPS-mediated iNOS COX-2 expression. In addition, TY-NS-B attenuated production of inflammatory cytokines such as TNF-α and IL-1β induced by LPS. TY-NS-B blocked LPS-mediated inhibitor of IκB-α, and inhibited p65 translocation to the nucleus and NF-κB activation. Furthermore, TY-NS-B reduced the phosphorylation of MAPKs such as p38 and JNK, but not ERK1/2. In addition, TY-NS-B increased ATF3 expression and ATF3 knockdown by ATF3 siRNA attenuated TY-NS-B-mediated inhibition of pro-inflammatory mediator expression. Collectively, our results suggest that TY-NS-B exerts potential anti-inflammatory effects by suppressing NF-κB and MAPK signaling activation, and increasing ATF3 expression. These findings indicate that TY-NS-B could be further developed as an anti-inflammatory drug.