Effects of Citalopram on frontal cortical neurons' bax mRNA bcl-2 mRNA expression and cell apoptosis of rat after stress.
- Author:
Ai-yue YU
;
Xiao-hong SUN
;
Xue-hong LIU
;
Jin ZHOU
;
Lan WANG
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Citalopram; pharmacology; Male; Neurons; drug effects; metabolism; Prefrontal Cortex; cytology; Proto-Oncogene Proteins c-bcl-2; metabolism; RNA, Messenger; Rats; Rats, Sprague-Dawley; Stress, Physiological; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Applied Physiology 2015;31(5):455-461
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of Citalopram on the mRNA expression of bax and bel-2 in frontal cortical neurons and on cell apoptosis of rats after stress.
METHODSTwenty-four healthy male SD rats were randomly divided into three groups (n = 8). The control group did no receive any treatment, the stress group was subject to stress and given normal saline and experimental group was given Citalopram irrigation stomach after stress. Rats were forced to swim to establish chronic stress model (15 min/d, 4 weeks), bax, bcl-2 mRNA expression were tested by in situ hybridization technique (ISH), TUNEL assay was used to determine cell apoptosis, Nikon image analysis software were used to measure the number of positive cells in each index.
RESULTSCompared with the control group, the stress group showed a larger number of bax mRNA expressing cells( P < 0.01), a smaller number of bcl-2 mRNA expressing cells (P < 0.01), and the staining intensity of positive cells was significantly reduced( P < 0.01). Compared with the stress group, the experiment group showed more reduced number of bax mRNA positive cells( P < 0.01) and significantly increased bcl-2 mRNA positive cells( P < 0.05), a small amount of positive cells were found, compared with that in the stress group, nuclear condensation in the experimental group was reduced significantly and the staining was obviously weaker( P < 0.01).
CONCLUSIONCitalopram significantly antagonizes bax mRNA and potentiatesbcl-2 mRNA protein expression and inhibits apoptosis of rat prefrontal cortical neurons caused by chronic stress, which might be one possible mechanism of Citalopram for prevention and treatment of psychosis caused by chronic stress.