| Objective:To establish a model of rats with experimental chronic colitis. To investigate the influence of inflammation on visceral sensitivity in experimental chronic colitis rats, and the mechanism of paroxetine reducing hypersensitivity in rats.Methods:48 male SD rats were randomly divided into two groups: 24 rats (group I) drunk with dextran sulfate sodium 5 days and then drunk with distilled water 7 days which induced experimental chronic colitis. After model was built, group I was divided into group A which intragastric with paroxetine by 2mg/Kg.d for 14 days and group B which intragastric with distilled water. Others were control group (group II), which drunk with distilled water for 12 days, then further divided into group D intragastriced with water and group C intragastriced with paroxetine by the same dose of group A. Then a ballonet was put into colon of every rat. We observed the abdominal withdrawal reflex(AWR) of rats at different levels of colorectal distension(CRD).The expression of c-Fos,substance P(SP), calcitonin gene-related peptide(CGRP) in spine cord were observed by the immuno-fluorescence staining after CRD.Results:The AWR scores of group B was significantly higher than other 3 groups P <0.01). There was no significant difference between colitis rats deal with paroxetine and noninflammatory rats. Fos SP CGRP average gray scale of group B were higher than those in group A C and D(P <0.05). Compared with noninflammatory rats, Fos and SP average gray scale of group A was no significant difference, while CGRP average gray scale was higher those in group C and group D.( P﹤0.05). The AWR scores and average gray scale of Fos, SP, CGRP were no difference between group C and group D. Conclusion:Our results demonstrate that inflammation significantly alters GI sensitivity in rats, and paroxetine can decrease the expression of Fos,SP,CGRP in spine cord which may alter the visceral sensitivity.
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