Activation of the Notch signaling pathway promotes neurovascular repair after traumatic brain injury.

The Notch signaling pathway plays a key role in angiogenesis and endothelial cell formation, but it remains unclear whether it is involved in vascular repair by endothelial progenitor cells after traumatic brain injury. Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs. Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells. Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells. Activation of the Notch signaling pathway in vivo in a rat model of mild traumatic brain injury promoted neurovascular repair. These findings suggest that the activation of the Notch signaling pathway promotes blood vessel formation and tissue repair after brain trauma.

Formalin inflammatory pain induced hippocampal neuronal apoptosis of rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate whether formalin inflammatory pain can induce hippocampal neuronal apoptosis of rats or not.</p><p><b>METHODS</b>Rats were subcutaneously injected with 0.2 ml 0.5% formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The flinches of rats were counted to observe their painful reaction. Flow cytometry was used to assay the ratio of apoptosis of hippocampal neurons. The immunohistochemistry was used to observe the expression of p53 protein in hippocampal subregions.</p><p><b>RESULTS</b>Compared with control group, the apoptotic ratio of hippocampal neurons was significantly increased in rats with inflammatory pain, and formalin inflammatory pain induced upregulation of p53 protein expression in all hippocampal subregions. Both the apoptotic ratio and the p53 protein expression peaked on the third day after the formalin injection. The twice injection of formalin into the hind paws of rats resulted in an enhancement of painful reaction and increase in apoptotic ratio of hippocampal neurons compared with the rats of injection formalin once group.</p><p><b>CONCLUSION</b>Formalin inflammatory pain can induce the hippocampal neuronal apoptosis in rats with a certain time course. Neuronal apoptosis is relevant to the intensity of pain. The up-regulation of p53 protein expression may implicate in the induction of hippocampal neuronal apoptosis in rats with inflammatory pain.</p>