ABSTRACT
<p><b>BACKGROUND</b>Proneurotrophins such as the precursor of nerve growth factor (proNGF) and the precursor of brain-derived neurotrophic factor (proBDNF) interacted with sortilin and p75(NTR) to form a complex capable of activating an apoptotic signaling. We found that the expression of p75(NTR) and sortilin was increased in ischemic retina induced by elevated intraocular pressure (IOP), but the protein expression changes of proNGF and proBDNF in the same situation were not clear. This study aimed to ascertain the protein expression changes of proNGF and proBDNF in ischemic retina induced by elevated IOP.</p><p><b>METHODS</b>Expression of proBDNF and proNGF was examined by double-labeling immunochemistry in normal rat retina, examined using Western blotting and analyzed using statistical methods in ischemic retina induced by elevated IOP.</p><p><b>RESULTS</b>Immunocytochemistry showed that the proBDNF expressed in the ganglion cell layer (GCL) while the proNGF primarily existed in both the nerve fiber layers (NFL) and large ganglion cell bodies of normal rat retina. Western blotting analysis demonstrated that the molecule weights of 28 kD (proBDNF)/25 kD (proNGF) band were increased significantly (P < 0.05) at days 3, 5 and 7 after retinal elevated-IOP-induced ischemia.</p><p><b>CONCLUSION</b>ProBDNF expressed in the GCL and proNGF primarily presented in NFL and large ganglion cell bodies of normal rat retina, the protein expression forms of 28 kD proBDNF and 25 kD proNGF increased in ischemic retina induced by elevated IOP.</p>
Subject(s)
Animals , Male , Rats , Blotting, Western , Brain-Derived Neurotrophic Factor , Immunohistochemistry , Intraocular Pressure , Physiology , Ischemia , Metabolism , Nerve Growth Factor , Protein Precursors , Rats, Wistar , Retinal Diseases , MetabolismABSTRACT
@#ObjectiveTo evaluate the biocompatibility of a kind of scaffolding material,Injured Nerve Regenerated Materid(INRM), which play the roles of regeneration of nerve after traumatic brain injury.MethodsINRM scaffolding material were transplanted into cortex of rats after traumatic injury.The brain coronal sections were stained for Nissel, astrocyte and microglia at 1 week, 1 month, and 2 months after injury.ResultsThe presence of INRM did not alter patterns of astrocyte compared with the control group (detected with antibodies against GFAP) at any time point; but decreased the expression of microglias (detected with antibodies against OX42) compared with the control group.ConclusionThe biomaterial INRM is well suited as a biocompatible scaffold material for the repair of brain injury in the brain.