Protection mechanisms of ATP-sensitive K channels on hippocampal CA1 neurons during chronic severe hypoxia.
- Author:
Lian-Yan HUANG
1
;
Wen-Jun LI
;
Bo-Xing LI
;
Fei ZOU
Author Information
- Publication Type:Journal Article
- MeSH: Adenosine Triphosphate; metabolism; Animals; Apoptosis; Cell Hypoxia; Cell Survival; Diazoxide; pharmacology; Genes, p53; Hippocampus; cytology; metabolism; KATP Channels; antagonists & inhibitors; metabolism; Neurons; cytology; metabolism; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Tolbutamide; pharmacology
- From: Chinese Journal of Applied Physiology 2007;23(3):257-261
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the protection mechanisms of K(ATP) channels on hippocampal CA1 neurons during chronic severe hypoxia.
METHODSp53 expression, DNA fraction, and cell apoptosis were examined in cultured hippocampal neurons in control group, hypoxia group, hypoxia group treated with K(ATP) channels antagonist and hypoxia group treated with K(ATP) channels agonist.
RESULTSIn the group of a 12 h long exposure to oxygen concentration of 0%, diazoxide (100 micromol/L), the K(ATP) channels agonist, reduced p53 expression and the hypoxia-induced apoptosis. In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.
CONCLUSIONK(ATP) channels protect hippocampal neurons against chronic severe hypoxia by suppressing p53 expression.
