Fig. 7

A CCR7 peptide designed to disrupt the CCL19‒CCR7 axis reduces IRI. A Schematic representation of CCR7. B Prediction of the structure of the CCR7 N-terminus via AlphaFold2. C Predicted binding conformation of the CCL19-CCR7 N-terminal heterodimer. D Potential peptide fragments of the CCR7 peptide 28–33. E Prediction of the binding site for the CCR7 peptide 28–33. F Representative TTC-stained sections 24 h after tMCAO in the vehicle, three different dosages of the CCR7 peptide 28–33 (5, 15, and 45 mg/kg), and edaravone groups, followed by an analysis of infarct volume. n = 7 animals in the sham group, three different dosages of CCR7 peptide 28-33 (5 mg/kg, 15mg/kg, and 45 mg/kg) group; n = 6 animals in the edaravone group. G, H The levels of the inflammatory factors TNF-α and IFN-γ in the peri-infarct area 24 h after tMCAO in the vehicle, CCR7 peptide 28–33 (15 mg/kg) and edaravone groups. n = 6/group. I Modified neurological severity scores of the vehicle, CCR7 peptide 28–33 (15 mg/kg), and edaravone groups at 24 h after stroke. n = 8/group. J‒L Functional recovery in the vehicle, CCR7 peptide 28–33 (15 mg/kg), and edaravone groups was assessed by the grid walking test (J), cylinder test (K), and adhesive removal test (L) at baseline and on day 4 and 7 after tMCAO. n = 7/group. The data are presented as the means ± SEMs. **P < 0.01; ***P < 0.001; ^#P < 0.05; ^##P < 0.01; ^###P < 0.001, ^†P < 0.05; ^††P < 0.01