4.7 Article

The protective effects of natural product tunicatachalcone against neuroinflammation via targeting RIPK2 in microglia BV-2 cells stimulated by LPS

期刊

BIOORGANIC & MEDICINAL CHEMISTRY
卷 69, 期 -, 页码 -

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bmc.2022.116916

关键词

Tunicatachalcone; RIPK2; Neuroinflammation; Natural product

资金

  1. National Natural Science Foundation of China [82104195]
  2. Hebei Province High School Science and Technology Research Project [QN2019118, QN2019121]
  3. Natural Science Foundation of Hebei Province [H2019206205, H2019206249]

向作者/读者索取更多资源

The study revealed that tunicatachalcone (TC) could alleviate neuroinflammation induced by microglia through the inhibition of RIPK2. This finding provides a new therapeutic target for neurologic disorders associated with inflammation.
Microglia-induced neuroinflammation plays a critical role in neurological diseases. At present, RIPK2 is considered to participate in inflammatory and autoimmune cellular pathways and diseases. RIPK2 is found to be a pivotal therapeutic target in neurologic disorders related to inflammation. In our research, we discovered the protective function of tunicatachalcone (TC) against neuroinflammation. TC is a natural chalcone compound derived from Pongamia pinnata, a medicinal plant. The results revealed that TC (5-20 mu M) ameliorated the activation of BV-2 microglia induced by lipopolysaccharide (LPS) in a dose-dependent way, which was proved by the reduced production of inflammation-related mediators. By using SPR-LC-MS/MS analysis, we revealed the potent inhibitory function of TC against neuroinflammation mediated by microglia via targeting RIPK2. A strong binding between TC and RIPK2 was further demonstrated based on the results of SPR, MST and molecular modeling. Through applying mRNA transcriptomics and bioinformatics analysis, it was demonstrated that TC could mediate RIPK2-dependent gene transcription to exert the neuroprotective effect. In summary, our research presented that RIPK2 was a possible therapeutic target of TC.

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