The expression of TGF-β1 and neurons apoptosis in injured brain tissue of neonatal rats caused by hypoxia and ischemia

AimTo study the sequential changes of the expression of TGF-β 1 and neurons apoptosis following hypoxia and ischemia(HI)in the cerebral cortex and hippocampus of the neonatal rat brain for further investigating the pathogenesis of neonatal cerebral injury. MethodsAn animal model of neonatal hypoxic and ischemic brain damage was set up by ligating the unilateral carotid artery of 7-day-old SD rats and keeping the rats in a hypoxic environment (8% oxygen) for 2 hours. The rats' brain tissues were collected at different time. Hematoxylin-eosin staining, terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL) staining and immunohistochemistry was used to detect neurons apoptosis and the expresson of TGF-β1 in the cerebral cortex and hippocampus, respectively. ResultsOur results showed that the expresson of TGF-β1 in the cerebral cortex and hippocampus began at 8 hours, peaked separately at 12 hours and 48 hours after hypoxia and ischemia. No apoptotic signals could be found in the control group. Neuron apoptosis 24 hours after hypoxia and ischemia was much more than that in the control group. Conclusion These results indicate that the expressed ion increase of TGF-β1 may be induced by neonatal hypoxia and ischemia. It indicated that TGF-β1 may regulate the apoptosis, and play a very important role in preventing neurons from injury following cerebral hypoxia and ischemia.