Preventive function of citalopram on neuro-cell apoptosis caused by long-term stress in CA1 and CA3 region of hippocampus / 中国病理生理杂志

ABSTRACT

AIM:To explore the preventing effect of citalopram on neuro-cell apoptosis caused by long-term stress in CA1 and CA3 region of hippocampus.METHODS:Forty male Sprague Dawley(SD)rats were randomly divided into five groups including blank group,control group(the control group was filled the stomade by 0.9% saline)and three experimental groups(intragastric administration of citalopram hydrobromide at doses of 8 mg?kg-1?d-1,4 mg?kg-1?d-1,1 mg?kg-1?d-1,respectively).Rat stress model was made by compulsory swimming everyday for 4 weeks.Cell apoptosis in CA1 and CA3 region of hippocampus was observed by HE staining method.Apoptotic cell numbers and integral optical density in CA1 and CA3 region were tested and analyzed by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL)method and Norton Internet Security BR(NIS BR)software.t-test was applied to compare apoptosis cell numbers and integral optical density.RESULTS:Control rats showed more static time and less struggling times.Conversely,static time was shorter and rats spent more time after exhaustive exercise,and more struggling times in the experimental group.Rats in control group showed more positive cells in CA1 and CA3 regions and higher integral optical density in CA3 region than those in blank group.Rats in experimental groups showed fewer positive cells in CA1 and CA3 regions.Rats in experimental group 1 and group 3 showed higher integral optical density in CA1 and CA3 regions than that in control group.CONCLUSION:Long-term stress might cause neuro-cell apoptosis in CA1 and CA3 region of hippocampus.Citalopram might have prophylactic effect on apoptosis caused by long-term stress in CA1 and CA3 region,and the prophylactic effect might not be influenced by citalopram.Our study suggests that the treatment mechanism of citalopram in neural and mental illness by long-term stress may involve in a major role by antagonizing neuronal apoptosis in both the CA1 and CA3.