ABSTRACT
BACKGROUND:Recovery of motor and sensory function from peripheral nerve injury is relatively slow and incomplete. It is a difficult problem for orthopedic surgeons that mainly leads to the decline in the quality of life in patients. OBJECTIVE: To conclude the methods and corresponding outcomes in peripheral nerve regeneration by analyzing the new treatment means for peripheral nerve injury. METHODS:PubMed, Wanfang, CNKI databases were retrieved for relevant articles using key words of “nerve injury, regeneration”, and then retrieval data were sorted and analyzed. RESULTS AND CONCLUSION:In recent years, in-depth studies on peripheral nerve repair have been made in the folowing aspects: surgical mode, drug, cytokine, gene transfer and biomaterials as wel as traditional Chinese medicine. If the detect size is four times longer than the diameter of nerves, the nerve regeneration chamber can achieve good outcomes. The methods of restoring nerve continuity folowing nerve injury are developed from surgical anastomosis to photochemohistological method, thermal laser welding, plastic repair and other emerging technologies. Studies have found that plasminogen activator, nerve growth factor, neurotrophic factor, recombinant erythropoietin, human tissue kalikrein, B vitamins and their derivatives, herbal preparations, immunosuppressive agents al can promote nerve regeneration.
ABSTRACT
BACKGROUND:Studies have shown that craniocerebral injury can promote the repair of sciatic nerve injury in rats, but its precise mechanism remains unclear. OBJECTIVE:To further explore the action mechanism of craniocerebral injury on the repair of sciatic nerve injury using morphology and histology. METHODS:Sixty specific-pathogen-free healthy male Sprague-Dawley rats were randomly divided into two groups. Rats with craniocerebral injury and sciatic nerve injury were considered as the experimental group. Rats with simple sciatic nerve injury were considered as the control group. Classical Feeney method was used in models of craniocerebral injury and SunderlandV sciatic nerve injury. At 8 and 12 weeks after modeling, sciatic nerve index was detected. Masson staining and NF200 immunofluorescence staining were used to observethe nerve regeneration atthe anstomotic site. Transmission electron microscope was used to observe the number of regenerative axons. RESULTS AND CONCLUSION:At 8 and 12 weeks after modeling, compared with the control group, gait and sciatic nerve index recovered better in the experimental group. In the experimental group, Masson staining showed fewer nerve membrane colagen fibers, and the axon arranged neatly.NF200 immunohistochemistry showed that in the experimental group, the density of regenerated nerves was high, and nerveswere regularly distributed. Transmission electron microscopy showed that in the experimental group, regenerative axons were regularly arranged, colagen scar was less, and myelin layer arranged regularly. Results suggested that the craniocerebral injury in rats may promote the repair of peripheral nerve injury by reducing scar colagen in nerve endings.