Abstract
Inhibition of RhoA/Rock could promote axon growth and alleviate optic nerve injury. However, the role of RhoA/Rock in the traumatic retinal nerve in vivo was not completely clear. In this study, we established a rabbit model of traumatic retinal nerve injury, and primary retinal ganglion cells (RGCs) were isolated and cultured under hypoxia-hypoglycemia condition that was mock to the microenvironment in the injured retinas in vivo. The Rock inhibitor fasudil was used to treat primary RGCs and ear vein injected into the model rabbits in vivo. RhoA/Rock signaling was activated in the injured optic nerve in rabbits. Western blotting analysis showed that RhoA/Rock signaling in the retina was activated during the traumatic optic neuropathy. Data on gene expression examination and Annexin V/PI dual staining combined with flow cytometry analysis displayed that fasudil injection reduced expression of Rho/Rock and apoptotic genes, as well as the apoptosis of RGCs in traumatic retinal nerve injury in vitro and in vivo. Moreover, fasudil injection reduced expression of Rho/Rock and apoptotic genes, as well as the apoptosis of RGCs in the rabbits with traumatic retinal nerve injury in vivo. In conclusion, fasudil treatment could significantly reduce the apoptosis of RGCs and relieved retinal nerve injury in vitro and in vivo.
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