Craniocerebral injury promotes sciatic nerve regeneration
10.3969/j.issn.2095-4344.2016.27.016
- VernacularTitle:颅脑损伤促进的坐骨神经再生
- Author:
Xinze HE
;
Wei WANG
;
Jianjun MA
;
Tiemin HU
;
Changyu YU
;
Yunfeng GAO
;
Xinglong CHENG
;
Pei WANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2016;20(27):4061-4067
- CountryChina
- Language:Chinese
-
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.