摘要
目的探讨帕罗西汀对结肠低度炎症(low grade mucosal inflammation,LGMI)大鼠内脏敏感性的影响及机制。方法将48只SD大鼠按是否诱导出结肠低度炎症分为2大组:每组24只,建模方式为8%葡聚糖硫酸钠(DSS)自由饮用5天,再予蒸馏水饮用7天。每组再按是否予帕罗西汀干预细分为2小组:每组12只,干预方式为2 mg.kg-1.d-1连续灌胃14天。通过结肠内置气囊进行结肠扩张实验(CRD),观察大鼠腹肌收缩反射(AWR)并评分。处死大鼠,免疫组化法观察腰骶部脊髓c-Fos蛋白、P物质(SP)、降钙素基因相关肽(CGRP)表达情况。结果与非炎症组相比,低度炎症组大鼠的AWR评分及c-Fos、SP、CGRP表达均有显著升高(P<0.05)。使用帕罗西汀干预后,低度炎症组大鼠的AWR评分、c-Fos、SP的表达与空白对照组无显著差异,而CGRP的表达仍比空白组显著升高(P<0.05)。结论低度炎症可增加大鼠结肠的内脏敏感性,帕罗西汀可以降低结肠低度炎症大鼠的内脏敏感性,其机制可能与抑制脊髓水平c-Fos、SP、CGRP信号传递有关。
Objective To investigate the effect and mechanism of paroxetine on visceral sensitivity in rats with low grade colonic mucosal inflammation.Methods Forty-eight male SD rats were randomly divided into two groups by means of whether established low grade mucosal inflammation（LGMI）,which induced by drank with dextran sulfate sodium 5 days and then drank with distilled water 7 days.Then each group was further divided into another two groups,which one was intragastric administration with paroxetine by 2 mg·kg-1·d-1 for 14 days and the other intragastric administration with distilled water.A ballonet was put into colon of every rat.The abdominal withdrawal reflex（AWR） of rats at different levels of colorectal distension（CRD） was observed.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,the expressions of c-Fos,SP and CGRP in LGMI group were significantly higher than those in noninflammatory group（P0.01）.There was no significant difference in AWR scores,the expression of c-Fos,SP between LGMI group and control group after paroxetine intervention.The expression of CGRP in LGMI group was higher than that in control group（P0.05）.Conclusion The results demonstrate that low grade mucosal inflammation significantly alters GI sensitivity in rats,and paroxetine can decrease the expressions of c-Fos,SP,CGRP in spine cord which may alter the visceral sensitivity.
出处
《胃肠病学和肝病学杂志》
CAS
2010年第12期1102-1105,1109,共5页
Chinese Journal of Gastroenterology and Hepatology
基金
福建省自然科学基金研究项目(2009J01138)
