Acute brain injuries and neuronal apoptosis
- VernacularTitle:急性颅脑损伤和神经元凋亡
- Author:
Na LIU
;
Zhiyang SUN
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(41):190-192
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: Controversy over the presence of neuronal apoptosis in acute brain injuries has not been resolved due to the lack of direct evidence. In this article, the authors briefly review the current research progress of apoptosis and discuss the relationship between acute brain injuries and neuronal apoptosis.DATA SOURCES: A computer-based retrieval for relevant papers with abstracts indexed in Medline database published in English full text between January 1995 and February 2005 was conducted using the key words of "acute brain injuries" and "Neuronal apoptosis". Related articles in Chinese full text published between January 2000 and December 2004 were also searched in Chinese periodical full text database, Wanfang databases with key words of "acute traumatic brain injury, neuronal apoptosis".STUDY SELECTION: The retrieved articles were first examined to exclude review articles and repetitions, and only randomized and non-randomized controlled experiments or clinical trials on acute traumatic brain injury and neuronal apoptosis were included.DATA EXTRACTION: Altogether 136 articles directly related to acute traumatic brain injury and neuronal apoptosis were collected, among which 19 met the inclusion criteria with the other 117 removed for repetition or irrelevancy.DATA SYNTHESIS: The valid articles were reviewed to identify the factors related to neuronal apoptosis, apoptotic network theory, detection methods of apoptosis, and the relationship between acute traumatic brain injury and neuronal apoptosis as well as the possible mechanisms.CONCLUSION: Neuronal apoptosis occurs after acute traumatic brain injury, which induces intrinsic and extrinsic neuronal environment changes including increased extracellular excitatory amino acid content, massive free radical production and abnormal gene expression. These factors interact with each other and modulate neuronal apoptosis through multiple pathways.
