Relationship between programmed cell death mechanisms and neuronal necrosis induced by seizures.
- Author:
Ren-zhe AN
1
;
Yong-ri YIN
;
Chun-ji JIN
;
Zheng JIN
;
Gen-huan LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Hippocampus; chemistry; pathology; In Situ Nick-End Labeling; Male; Proto-Oncogene Proteins; analysis; Proto-Oncogene Proteins c-bcl-2; analysis; Rats; Rats, Sprague-Dawley; Seizures; chemically induced; physiopathology; bcl-2-Associated X Protein
- From: Chinese Journal of Pediatrics 2003;41(4):290-292
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons.
METHODSSeizure was induced by pilocarpine (P) in Sprague-Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion-fixation. Neuronal death was assessed by light microscopy with the hematoxylin-eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Bax and Bcl-2 protein expression were examined by histochemistry.
RESULTSTwenty-four and 72 hours after seizures, neuronal death in hippocampus CA1 region was morphologically necrotic. TUNEL-positive and morphologically necrotic cells increased in the hippocampal CA1 region at 72 hours after seizures, there was significant difference compared with controls (P < 0.001). Bax expression was also increased in the hippocampal CA1 region at 72 hours after seizures (P < 0.001), but Bcl-2 expression did not increase, while Bcl-2/Bax ratio decreased.
CONCLUSIONSeizures induced late-onset neuronal necrosis was accompanied by programmed cell death mechanisms.
