Research Paper Volume 13, Issue 14 pp 19048—19063

Combined treatment with C16 peptide and angiopoietin-1 confers neuroprotection and reduces inflammation in 3-nitropropionic acid-induced dystonia mice


Figure 10. Treatment with C16+Ang-1 reduces neuronal apoptosis, vascular leakage and blood-brain barrier permeability. (AC) Electron micrographs showing ultrastructural morphology of the normal group. (A) Normal neurons with well-defined nuclei and dispersed chromatin (euchromatin). (B) Blood vessels have intact tight junctions. There was no tissue edema or blood vessel leakage. (C) Normal myelinated axons. (DF) Changes in ultrastructural morphology in the 3-NP-treated group. (D) Neuronal apoptosis was evidenced by nuclei with condensed, fragmented, and marginated chromatin against the nuclear envelope compared with normal cells. (E) Leakage from severe blood vessels and tissue edema in the extracellular space. (F) Myelin sheath splitting, loosening, and fusion, and vacuoles were observed. (GI) In the 3-NP+C16+Ang-1 group, the morphology of (G) nuclei was relatively normal. (H) Perivascular edema and (I) myelin sheath splitting were reduced.