Vibsanin B preferentially targets HSP90β, inhibits interstitial leukocyte migration, and ameliorates experimental autoimmune encephalomyelitis.

نویسندگان

  • Bai-Xin Ye
  • Xu Deng
  • Li-Dong Shao
  • Ying Lu
  • Run Xiao
  • Yi-Jie Liu
  • Yi Jin
  • Yin-Yin Xie
  • Yan Zhao
  • Liu-Fei Luo
  • Shun Ma
  • Ming Gao
  • Lian-Ru Zhang
  • Juan He
  • Wei-Na Zhang
  • Yi Chen
  • Cheng-Feng Xia
  • Min Deng
  • Ting-Xi Liu
  • Qin-Shi Zhao
  • Sai-Juan Chen
  • Zhu Chen
چکیده

Interstitial leukocyte migration plays a critical role in inflammation and offers a therapeutic target for treating inflammation-associated diseases such as multiple sclerosis. Identifying small molecules to inhibit undesired leukocyte migration provides promise for the treatment of these disorders. In this study, we identified vibsanin B, a novel macrocyclic diterpenoid isolated from Viburnum odoratissimum Ker-Gawl, that inhibited zebrafish interstitial leukocyte migration using a transgenic zebrafish line (TG:zlyz-enhanced GFP). We found that vibsanin B preferentially binds to heat shock protein (HSP)90β. At the molecular level, inactivation of HSP90 can mimic vibsanin B's effect of inhibiting interstitial leukocyte migration. Furthermore, we demonstrated that vibsanin B ameliorates experimental autoimmune encephalomyelitis in mice with pathological manifestation of decreased leukocyte infiltration into their CNS. In summary, vibsanin B is a novel lead compound that preferentially targets HSP90β and inhibits interstitial leukocyte migration, offering a promising drug lead for treating inflammation-associated diseases.

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عنوان ژورنال:
  • Journal of immunology

دوره 194 9  شماره 

صفحات  -

تاریخ انتشار 2015