Fig. 7: Electron microscopy revealed the ultrastructural morphology of the striatum in each group.
Scale bar = 2 μm. normal neuronal nuclei with uncondensed chromatin (a). Normal myelinated axons with dark, ring-shaped myelin sheaths surrounding axons, and typically shaped mitochondria with clear cristae (blue arrow in b). The normal control group showed no tissue edema or blood vessel leakage (c) but had intact tight junctions (d). No inflammatory cell infiltrate was found in normal tissues (e). The neurons in the vehicle-treated PD model group had shrunken nuclei with condensed, fragmented, and marginated nuclear chromatin (f). mitochondria vacuolization with swollen cristae (blue arrow in g). Severe vascular vessel leakage and tissue edema were detected in the extracellular space surrounding blood vessels (h). The tight junctions between the endothelial cells were lost (black arrow in i). Inflammatory cell infiltration was observed surrounding blood vessels (red arrow in j). However, in C16 (k–o), Ang-1 (p–t), and C16 plus Ang-1 treated groups (u–y), the morphology of the nuclei (k, p, u), myelin, and axons (l, q, v) were relatively normal. Perivascular edema (m, r, w) was alleviated. The morphology of the tight junctions (n, s, x) was also relatively normal, especially in the groups treated with Ang-1 alone or in combination with C16 (s, x). The morphology of the mitochondria was relatively normal (blue arrows in l, q, and v). Inflammatory cell infiltration (red arrows in o, t, y) was mainly detected within blood vessels in the C16 alone and C16 plus Ang-1 groups (o, y), and was reduced in Ang-1-treated group (t) when compared with the model animals (j). PD, Parkinson’s disease; C16, peptide (KAFDITYVRLKF) that can selectively bind integrin ανβ3; Ang-1, angiopoietin-1.
