A Dalbergia odorifera extract improves the survival of endotoxemia model mice by inhibiting HMGB1 release

BMC Complementary and Alternative Medicine

Research Article

Taesik Yoo¹  Han Geuk Seo¹  Jung Seok Hwang¹  Hyuk Soo Choi¹  Chi-Ho Lee¹  Won Jin Lee¹  Sun Ah Ham¹  Kyung Shin Paek²  Ho-Chul Shin³  Jin-A Park³ 

[1] College of Animal Bioscience & Technology, Konkuk University, 120 Neungdong-ro, 05029, Gwangjin-gu, Seoul, Korea;Department of Nursing, Semyung University, Semyung-ro, 390-711, Jechon, Chungbuk, Korea;Department of Veternary Pharmacology and Toxicology, College of Veterinary Medicine, Konkuk University, 120 Neungdong-ro, 05029, Gwangjin-gu, Seoul, Korea;

关键词: Dalbergia Odorifera;    Endotoxemia;    HMGB1;    Inflammation;    Nitric oxide;   

DOI  :  10.1186/s12906-017-1725-0

 received in 2016-09-01, accepted in 2017-04-05,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundDalbergia odorifera T. Chen (Leguminosae) is an indigenous medicinal herb that is widely used as a popular remedy in northern and eastern Asia. However, the cellular mechanisms underlying the biological activity of D. odorifera are not fully elucidated.MethodsAnti-inflammatory effect of D. odorifera extract (DOE) was determined through intraperitoneal injection in a mouse model of endotoxemia induced by lipopolysaccharide (LPS). RAW 264.7 cells, a murine macrophage, were also treated with LPS to generate a cellular model of inflammation, and investigated the anti-inflammatory activity and underlying mechanisms of DOE and its constituent isoliquiritigenin.ResultsDOE dose-dependently inhibited LPS-induced release of high mobility group box 1 (HMGB1), a late proinflammatory cytokine, and decreased cytosolic translocation of HMGB1 in RAW264.7 cells. This inhibitory effect of DOE on HMGB1 release was observed in cells treated with DOE before or after LPS treatment, suggesting that DOE is effective for both treatment and prevention. In addition, DOE significantly inhibited LPS-induced formation of nitric oxide (NO) and expression of inducible NO synthase (iNOS) in a dose-dependent manner. These effects of DOE were accompanied by suppression of HMGB1 release triggered by LPS, suggesting a possible mechanism by which DOE modulates HMGB1 release through NO signaling.Isoriquiritigenin, a constituent of DOE, also attenuated LPS-triggered NO formation and HMGB1 release in RAW264.7 cells, indicating that isoriquiritigenin is an indexing molecule for the anti-inflammatory properties of DOE. Furthermore, c-Jun N-terminal kinase, but not extracellular signal-regulated kinase and p38, mediated DOE-dependent inhibition of HMGB1 release and NO/iNOS induction in RAW 264.7 cells exposed to LPS. Notably, administration of DOE ameliorated survival rates in a mouse model of endotoxemia induced by LPS, where decreased level of circulating HMGB1 was observed.ConclusionThese results suggest that DOE confers resistance to LPS-triggered inflammation through NO-mediated inhibitory effects on HMGB1 release.

【 授权许可】

CC BY   
© The Author(s). 2017