Degenerated Death And Protection Of Neurons Resulted By Ruptured Injury Of Axis-cylinders Or Dendrites

Several reasons influence plerosis after axis-cylinders or dendrites of neurons are injured Formerly investigations focused on damaged local but ignored roles of neuron body to plerosis of nerve injury. Recently years many experiments have observed that certain ectogenesis factors play an important role to protect neurons. Glial cell line-derived neurotrophic factor (GDNF) is one of neurotrophic factors (NTFs) kindred, which are a broad class of proteins that can facilitate nervous system phylogeny, protect and repair the injured neurons. Many of investigations have made clear that GDNF had tremendous potential to growth, development and regeneration of nerve system. But GDNF is unable to pass blood-brain barrier (BBB) and spinal cord barrier as a kind of protein. In this study, pseudotype virus mixture strains dvHSV-GDNF that is replication defective is structured and enclosed-based herpes simplex virus-I carrier. We investigate whether exogenous factors can protect injured neurons and want to find out the new pathway of damaged neurons' functional restoration from angle of cell body in this experiment We detected as follow these principal results.1. Death phenomenon of spinal cord anterior horn motoneurons caused by injury of sciatic nerve and scarification injury After sciatic nerve of adult wistar rats was key out in distancing from infrapiriform foramen o.5cm, on the 4th day quantities of motoneurons (MNs) of injured side spinal cord (SC) anterior horn is 80-85 percent of ones of left side. And on the 7th day, quantities of degeneration death MNs of injured side SC anterior horn is close to 30 percent Many of MNs in three groups has occurred degeneration deathon scarification injury the 1 st day.2. Protection effects of GDNF and HSV-GDNF to degenerated death of MNs caused by ruptured injury of axis-cylinder and dendrite Togroups applied GDNF or HSV-GDNF, quantities of immunologic reaction (TR) positive MNs in injured side of SC anterior horn are widespresd higher than ones of control groups on injury of sciatic nerve the 4th and 7tii day in vrvo(?<0.01). To the cultured MNs in vitro, we have gotten the similar outcome. GDNF or HSV-GDNF was oflFered to the cultured MNs while scarification injury was given performed. We observe that the quantities and apophysises of attached MNs in GDNF and HSV-GDNF groups are obviously higher lhan ones of control group on injury the 4th and 7th day (PO.05). These results suggest that GDNF and HSV-GDNF can prevent injured MNs from degeneration death.3. Effect of GDNF and HSV-GDNF on Bcl-2 expression in SC anterior horn MNs Bcl-2 is protein product of oncogene bcl-2. Bcl-2 gene is expressed in nerve system. Super-expression of neurons' bcl-2 gene can prevent neurons from apoptosis. In this study, effects of GDNF and HSV-GDNF on Bcl-2 expression in SC anterior MNs were observed with immunogistochemistry and DNA detect in situ method. The results show that quantities and average optical densit of Bcl-2-IR positive MNs of SC anterior horn in GDNF and HSV-GDNF groups is higher than ones of control group in not only injury of sciatic nerve experiment but also scarification injury experiment to cultured MNs. We conclude that application of exogenous GDNF and HSV-GDNF to transected sciatic nerve and injured MNs of SC anterior hom can prevent the massive neuron apoptosis or programmed cell death (PCD) induced by injury.From above statements, author thinks it as an important reason degeneration death (or apotosis) of portion neurons caused by axis-cylinders or dendrites transecting and we should sufficiently think highly of it Protecting neurons whose process is injured is a new method of rising post-injury neurons' functional recover. These posses a comprehensive prospect of clinical applicatioa...