Apoptosis and expression of apoptosis-related proteins in experimental different denervated guinea-pig facial muscle.
- Author:
Lian HUI
1
;
Hong-Quan WEI
;
Xiao-Tian LI
;
Chao GUAN
;
Zhong REN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Denervation; Facial Muscles; cytology; innervation; metabolism; Female; Guinea Pigs; Male; Proto-Oncogene Proteins c-bcl-2; metabolism
- From: Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2005;40(2):119-123
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study apoptosis and expression of apoptosis-related proteins in experimental different denervated guinea-pig facial muscle.
METHODAn experimental model was established with guinea pigs by compressing the facial nerve 30 second (reinnervated group) and resecting the facial nerve (denervated group). TUNEL method and immunohistochemical technique (SABC) were applied to detect the apoptosis and expression of apoptosis-related proteins bcl-2 and bax from 1st to 8th week after operation.
RESULTExperimentally denervated facial muscle revealed consistently increase of DNA fragmentation, average from(34.4 +/- 4.6)% to (38.2 +/- 10.6)%, from 1st week to 8th week after operation; Reinnervated facial muscle showed a temporal increase of DNA fragmentation, and then the muscle fiber nuclei revealed decreased DNA fragmentation along with the function of facial nerve recovered, latterly normal, average from (32.0 +/- 8.03)% to (5.6 +/- 3.5)%, from 1st week to 8th week after operation. In denervated group, bcl-2 and bax were expressed strongly; in reinnervated group, bcl-2 expressed consistently, but bax disappeared latterly along with the function of facial nerve recovered.
CONCLUSIONExpression of DNA fragmentation and apoptosis-related proteins in denervated muscle are general reaction to denervation. bcl-2 can prevent early apoptotic muscle fiber to survival until reinnervation. It is concluded that proteins control apoptosis may give information for possible therapeutic interventions to reduce the rate of muscle fiber death in denervated atrophy in absence of effective primary treatment.