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1.
Chinese Journal of Applied Physiology ; (6): 455-461, 2015.
Article in Chinese | WPRIM | ID: wpr-254991

ABSTRACT

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Twenty-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.</p><p><b>RESULTS</b>Compared 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).</p><p><b>CONCLUSION</b>Citalopram 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.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Citalopram , Pharmacology , Neurons , Metabolism , Prefrontal Cortex , Cell Biology , Proto-Oncogene Proteins c-bcl-2 , Metabolism , RNA, Messenger , Rats, Sprague-Dawley , Stress, Physiological , bcl-2-Associated X Protein , Metabolism
2.
Chinese Journal of Applied Physiology ; (6): 439-442, 2014.
Article in Chinese | WPRIM | ID: wpr-243466

ABSTRACT

<p><b>OBJECTIVE</b>To study the effects of citalopram on the expression of proliferating cell nuclear antigen (PCNA) and proto-oncogene protein (C-fos) and cell apoptosis in frontal cortical neurons of rat after stress.</p><p><b>METHODS</b>Twenty four healthy male SD rats were randomly divided into three groups (n = 8): control group, stress group (treated with saline, ig) , experimental group (treated with Citalopram 4 mg/kg x d for 28 days, ig). Rats were forced to swim to establish chronic stress model. The protein expression levels of PCNA and C-fos were tested by immunohistochemistry assay. TUNEL assay was used to test cell apoptosis. Nikon image analysis software was used to determine the number of positive cells in each index.</p><p><b>RESULTS</b>Compared with the control group, the stress group showed a smaller amount of PCNA-positive cells, a larger number of C-fos positive cells, and the volume of positive cells was significantly reduced. Compared with the stress group, the PCNA positive cells were increased significantly, the C-fos positive cells and TUNEL positive cells were decreased significantly, nuclear condensation phenomenon in frontal cortical neurons and the staining was significantly lighter in experimental group (P < 0.05).</p><p><b>CONCLUSION</b>Citalopram significantly antagonize PCNA, C-fos protein expression and cell apoptosis of rat prefrontal cortical neurons caused by chronic stress, which might be the one of mechanisms of citalopram for prevention and treatment of psychosis caused by chronic stress.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Citalopram , Pharmacology , Frontal Lobe , Cell Biology , Immunohistochemistry , Neurons , Cell Biology , Proliferating Cell Nuclear Antigen , Metabolism , Proto-Oncogene Proteins c-fos , Metabolism , Rats, Sprague-Dawley , Stress, Physiological
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