Research Paper Volume 15, Issue 16 pp 8315—8324
miR-100-5p activation of the autophagy response through inhibiting the mTOR pathway and suppression of cerebral infarction progression in mice
Figure 2. Overexpression of miR-100-5p could inhibit CI in mice. (A) HE staining results of the model, miR-100-5p KD, and miR-100-5p OE groups. In CI model group, a large number of ethmoid necrotic foci in ischemic cerebral tissue could be observed (arrowheads). The number of neurons in the necrotic foci was significantly reduced, with pyknosis and hyperchromatic nuclei; miR-100-5p KD aggravates the damage in cerebral while miR-100-5p OE attenuates the damage caused by CI. The CI volume was significantly reduced in the miR-100-5p OE group compared with the model group. (B) Overexpression of miR-100-5p inhibited apoptosis in the brain tissue of mice. TUNEL staining was performed, and the number of TUNEL-positive cells significantly declined in the miR-100-5p OE group compared with the model group. CI, cerebral infarction; HE, hematoxylin and eosin; NC, negative control; KD, knock down; OE, overexpression; TUNEL, terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling. *P<0.05, **P<0.01.