Synthesis and evaluation of 1,2,4-oxadiazole derivatives as potential anti-inflammatory agents by inhibiting NF-κB signaling pathway in LPS-stimulated RAW 264.7 cells

  • Bioorg Med Chem Lett. 2020 Sep 1;30(17):127373. doi: 10.1016/j.bmcl.2020.127373.
Yu-Ying Zhang  1 Qian-Qian Zhang  1 Juan Zhang  2 Jia-Li Song  1 Jia-Cheng Li  1 Ke Han  3 Jin-Tian Huang  4 Cheng-Shi Jiang  5 Hua Zhang  6
Affiliations
  • 1. School of Biological Science and Technology, University of Jinan, Jinan 250022, China.
  • 2. School of Biological Science and Technology, University of Jinan, Jinan 250022, China. Electronic address: [email protected].
  • 3. Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China.
  • 4. Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250021, China.
  • 5. School of Biological Science and Technology, University of Jinan, Jinan 250022, China. Electronic address: [email protected].
  • 6. School of Biological Science and Technology, University of Jinan, Jinan 250022, China. Electronic address: [email protected].
Abstract

In this study, a series of compounds with 1,2,4-oxadiazole core was designed and synthesized for the optimization of JC01, an anti-inflammatory hit identified from our in-house compound library using NF-κB pathway luciferase assay and NO production assay. All the synthetic compounds 1-29 have been screened for their anti-inflammatory effects by evaluating their inhibition against LPS-induced NO release, and compound 17 exhibited the highest activity. Western blotting and immunofluorescence analysis revealed that 17 prominently inhibited LPS-induced activation of NF-κB in RAW264.7 cells and blocked the phosphorylation of p65. Consistent with these results, it was found that 17 prevented the nuclear translocation of NF-κB induced by LPS. These data highlighted 17 as a promising anti-inflammatory agent by inhibiting NF-κB activity.

Keywords
1,2,4-oxadiazole; Anti-inflammatory activity; NF-κB; NO production; Structural optimization.