Error in Figure
In the original publication [1], there was a mistake in Figure 7 as published. In Figure 7, the magnification of subfigure D,H,L is different from other subfigures. The corrected Figure 7 appears below. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.
Figure 7.
Electron micrographs show the ultrastructural morphology of the (A–D) sham control, (E–H) vehicle, and (I–L) C + A groups. The sham control rats showed (A) neuronal nuclei with uncondensed chromatin (red arrow in (A)). There was (B) no tissue edema or blood vessel leakage (red arrow in (B)). Intact tight junctions (red arrow in (C)) and myelinated axons surrounded by dark, ring-shaped myelin sheaths were also observed (red arrows in (C,D)). In the vehicle group, (E) neuronal apoptosis was evidenced by shrunken nuclei with marginated, fragmented, and condensed nuclear chromatin (showed by two arrows in (E)). (F) Severe blood vessel leakage and tissue edema in the extracellular space surrounding the vessels (yellow arrow in (F)). (G) Loosening of tight junctions between the endothelium (purple arrow in (G)). (H) Myelin sheath loosening and splitting (green arrow in (H)). Treatment with C16 plus Ang-1 reduced morphological changes of the nuclei (orange arrow in (I)), alleviated perivascular edema (orange arrow in (J)), prevented destruction of tight junctions (orange arrow in (K)), and decreased myelin sheath splitting (orange arrow in (L)).
Reference
- Fu, X.; Wang, J.; Cai, H.; Jiang, H.; Han, S. C16 Peptide and Ang-1 Improve Functional Disability and Pathological Changes in an Alzheimer’s Disease Model Associated with Vascular Dysfunction. Pharmaceuticals 2022, 15, 471. [Google Scholar] [CrossRef] [PubMed]
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