摘要
目的:研究SF对大鼠乙酸性结肠炎的作用及其机制方法:利用乙酸灌肠制备大鼠结肠炎模型.实验设正常对照组,模型对照组,SF给药组(200 mg/kg,400 mg/kg, 800 mg/kg),每天灌肠给药1次,用药7 d.实验结束后评价大鼠结肠黏膜损伤指数(CMDI)与粪便隐血实验(OBT)、检测结肠组织MDA,NO,PGE2,TXB2含量;MPO, SOD活性;COX-2,NF-κBp65表达水平及血小板聚集率. 结果:模型组大鼠CMDI,OBT评分显著增加;MDA, NO,PGE2,TXB2含量,MPO活性,COX-2与NF- κBp65表达水平及血小板聚集率显著升高;而SOD活性显著降.SF灌肠改善模型组大鼠CMDI,OBT评分;使结肠组织MDA,NO,PGE2,TXB2含量,MPO活性,血小板聚集率不同程度降低,SOD活性升高,同时下调COX-2与NF-κBp65的过度表达.SF用药呈一定量效关系. 结论:SF通过抗氧化,抑制血小板活化、花生四烯酸代谢及NF-κB表达,缓解大鼠乙酸性结肠炎炎症反应,减轻结肠黏膜损伤.
AIM: To study the effects of sodium ferulate on acetic acid-induced rat colitis and its mechanism. METHODS: The colitis model of rats was produced by intracolon enema with acetic acid. The experiment animals were divided into 5 groups: normal group, model group, SF groups (200 mg/kg, 400 mg/kg, 800 mg/kg), and treated intracolonically with saline and SF respectively once per day for 7 days. At the end of the experiment, the colon mucosa damage index (CMDI) and the occult blood test (OBT) were evaluated.The contents of MDA, NO, PGE2, and TXB2, the activities of myelopexoxidase (MPO) and SOD, the expression of COX-2 and NF-κBp65 in the rat colon were detected. Platelet agglutinability was also measured. RESULTS: The extents of CMDI and OBT, the contents of MDA, NO, PGE2 and TXB2, the activity of MPO, the expression of COX-2 and NF-κBp65 in the colon and the platelet agglutinability in the model group were higher than those in normal group, while the activity of SOD was lower than that in normal group. SF could alleviate the CMDI and OBT, and ameliorate the abnormity of these detected indexes in a dose-depended manner. CONCLUSION: Treatment with SF intracolon can relieve the inflammation reaction, attenuate the colon mucosal damage in the rat colitis through resisting oxidative stress, restraining arachidonic acid metabolism, platelet activation and the expression of NF-κB.
出处
《世界华人消化杂志》
CAS
2004年第1期108-111,共4页
World Chinese Journal of Digestology
基金
湖北省科技攻关项目
No.2001AA308B~~