P75 neurotrophin receptor mRNA sequential expression and significance after Cauda equina compression in rats.
- Author:
Hao-peng LI
1
;
Yu LIU
;
Xi-jing HE
;
Si-yue XE
;
Jie CHEN
;
Dong-xu FENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Cauda Equina; Disease Models, Animal; Female; Polyradiculopathy; etiology; metabolism; RNA, Messenger; analysis; Rats; Rats, Sprague-Dawley; Receptor, Nerve Growth Factor; genetics; Spinal Cord Compression; metabolism
- From: China Journal of Orthopaedics and Traumatology 2011;24(6):509-513
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the mRNA expression of p75NTR (p75 neurotrophin receptor) and the amount of neuronal cells apoptosis in lumbar-sacral spinal cord at different time points after the acute cauda equina compression in rats and to explore their correlation.
METHODSSixty adult female Sprague Dawley(SD) rats were randomly divided into the normal control group and the compression groups. The acute cauda equine compression model was established as placing a silicon gel rubber at L(3,4) level of the vertebral canal which represented about 70% to 80% compression to the cross section. The whole L(1,2) level of spinal cords were harvested at 1, 3, 5, 7, 14, 28 d after operation in compression group. Tunel method was applied to observe cell apoptosis and RT-PCR was used to detect the p75NTR mRNA expression. SPSS 13.0 statistical software was adopted to help analysis.
RESULTSIn the compression group, both the nerve cells apoptosis and the p75 mRNA expression existed the trend of low-high-low synchronally compared with the control group, there was a significant difference (P < 0.05) among comprssion groups at different time points,there was a significant difference in changes (P < 0.05). p75NTR of mRNA expression and lumbosacral nerve cells apoptosis was in a positive correlation.
CONCLUSIONAfter acute cauda equina compression, p75NTR mRNA expression is closely related to the neuronal apoptosis, which plays an important role in the molecular mechanism of the CES.