Effects of mecobalamin on Bax and Bcl-2 in neurons after peripheral nerve injury.
- Author:
Dongqiang WANG
1
;
Pingping ZHANG
1
;
Zhijun LI
2
;
E-mail: DOCTORZHIJUN@ALIYUN.COM.
;
Ying LIU
1
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Male; Neurons; cytology; drug effects; Peripheral Nerve Injuries; metabolism; pathology; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Wistar; Sciatic Nerve; pathology; Spinal Cord; cytology; Vitamin B 12; analogs & derivatives; pharmacology; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2015;33(11):841-843
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effects of mecobalamin on the expression of apoptosis-related proteins, Bax and Bcl-2, in neurons after peripheral nerve injury, and to explore the role of neuron apoptosis in peripheral nerve regeneration after injury.
METHODSThirty healthy adult male wistar rats were randomly divided into sham-operation group, model group, and mecobalamin group, with 10 rats in each group. A rat model of left sciatic nerve semi-injury was established using forceps. Rats in the mecobalamin group were fed mecobalamin, while rats in the sham-operation group and model group were given the same dose of normal saline. The protein expression of Bax and Bcl-2 in neurons was measured at 14 days after operation. A semi-quantitative analysis of Bax and Bcl-2 proteins was performed by image analysis technology.
RESULTSThe model group had significantly increased Bax protein expression and significantly reduced Bcl-2 protein expression in spinal cord anterior horn motor neurons and ganglion sensory neurons compared with the sham-operation group (P<0.05). Compared with the model group and sham-operation group, the mecobalamin group had significantly reduced Bax protein expression and significantly increased Bcl-2 protein expression in spinal cord anterior horn motor neurons and ganglion sensory neurons (P<0.05).
CONCLUSIONMecobalamin has anti-apoptotic effect, and it contributes to neurological function recovery possibly by inhibiting the death of injured neurons.