Does inhibition of poly ( adenosine diphosphate-ribose ) polymerase decrease long-term histologic damage in testicular ischemia-reperfusion injury?
The results of this study show that PARP may have a role in the testicular damage caused by ischemia-reperfusion. Administering PARP inhibitors before reperfusion may have the potential to decrease the long-term histologic damage that occurs after testicular torsion.
Taken collectively these data indicate a broad overall down-regulation in the genes examined, including genes for neurotrophic/growth factor receptors as well as for several growth factors. There was a lack of a significant regenerative response, with the exception of an up-regulation of Atf3 and early up-regulation of Hspb1 (Hsp27), both involved in cell stress/neuroprotection as well as axonal regeneration. There was no indication of a cell death response over the first month post-injury. In addition, there appear to be significant phenotypic differences between uninjured TPS and LDPT neurons, which may partly account for the differences observed in their post-axotomy responses. The findings in this current study stand in stark contrast to the findings from our previous work on TPS neurons. This suggests that different approaches will be needed to enhance the capacity for each population of propriospinal neuron to survive and undergo successful axonal regeneration after SCI.