Abstract
The aim of the present study was to investigate the possible damage-repair mechanisms of neural stem cells (NSCs) following hypoxic-ischemic brain damage (HIBD). NSCs obtained from Sprague Dawley rats were treated with tissue homogenate from normal or HIBD tissue, and β‑catenin expression was silenced using siRNA. The differentiation of NSCs was observed by immunofluorescence, and semiquantitative reverse transcription‑polymerase chain reaction and western blot analysis were applied to detect the mRNA and protein expression levels of Ngn1 and BMP4 in the NSCs. Compared with control NSCs, culture with brain tissue homogenate significantly increased the differentiation of NSCs into neurons and oligodendrocytes (P<0.05), whereas differentiation into astrocytes was significantly reduced (P<0.05). Compared with negative control‑transfected cells, knockdown of β‑catenin expression significantly decreased the differentiation of NSCs into neurons and oligodendrocytes (P<0.01), whereas the percentage of NSCs differentiated into astrocytes was significantly increased (P<0.01). Compared with control NSCs, the mRNA and protein expression levels of Ngn1 were significantly increased (P<0.01) and BMP4 levels were significantly reduced (P<0.01) by exposure of the cells to brain tissue homogenate. Compared with the negative control plasmid‑transfected NSCs, the levels of Ngn1 mRNA and protein were significantly reduced by β‑catenin siRNA (P<0.01), whereas BMP4 levels were significantly increased (P<0.01). In summary, the damaged brain tissues in HIBD may promote NSCs to differentiate into neurons for self‑repair processes. β‑Catenin, BMP4 and Ngn1 may be important for the coordination of NSC proliferation and differentiation following HIBD.