[The relationship between expression of fas mRNA and apoptosis after traumatic brain injury in rats and the role of GM-1 in protecting the brain].
OBJECTIVE
To explore the mechanism of apoptosis after traumatic brain injury (TBI) in rats and elucidate the role of GM-1 by detecting the expression of Fas mRNA and apoptosis in hippocampi.


METHODS
After creating the model of Marmarou cranio-cerebral trauma and offering GM-1 therapy, we observed the expression of Fas mRNA and apoptotic cell death using in situ hybridization and terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) technique.


RESULTS
Increased expression of Fas mRNA and increased apoptotic cells in hippocampi after TBI were observed. GM-1 could decrease the expression of Fas mRNA and apoptotic cell death.


CONCLUSIONS
The increased expression of Fas mRNA may be a noteworthy cause of apoptotic cell death after traumatic brain injury. GM-1 may play a protective role by way of decreasing the expression of Fas mRNA and apoptotic cell death.
Liu
Qing-jun
QJ
Department of Neurosurgery, Affiliated Hospital of Northern China Coal Medical College, Tangshan 063000, China.
Zhu
Jun
J
Zhao
Jing-xia
JX
Li
Jian-min
JM
Fu
Ai-jun
AJ
Liu
Gang
G
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001930:Brain Injuries / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005677:G(M1) Ganglioside / Q000031:analogs & derivatives* / Q000494:pharmacology; D006624:Hippocampus / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D019014:fas Receptor / Q000096:biosynthesis* / Q000235:genetics
D018696:Neuroprotective Agents; D012333:RNA, Messenger; D019014:fas Receptor; C502266:ganglioside GM1alpha; D005677:G(M1) Ganglioside