摘要
为探讨龙血竭灌胃对葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎(UC)大鼠模型血小板活化的影响,本研究将60只SD大鼠随机分为A~E5组,A组为空白对照组,B组为模型对照组,C、D、E组分别为低、中、高剂量龙血竭治疗组;通过DSS建立UC大鼠模型,造模成功后,A、B组予生理盐水(4ml/只)灌胃,C、D、E组分别予600mg/kg、1200mg/kg、2400mg/kg龙血竭混悬液(4ml/只)灌胃,每天1次,连续7d;对比治疗后各组大鼠疾病活动指数(DAI);给药7d后在麻醉下取血检测血浆中血小板活化因子(PAF)和血小板因子4(PF4)的表达情况,并处死大鼠,观察组织学损伤(HI)情况。结果显示,治疗7d后,C~E组DAI、HI评分均明显低于B组,P〈0.05;C~E组各组间差异无统计学意义,P〉0.05。C~E组血浆中PAF、PF4含量均明显低于B组,P〈0.05;C~E组各组间差异无统计学意义,P〉0.05;C~E组血浆中PAF、PF4含量仍高于A组,P〈0.05。结果表明,龙血竭在一定程度上可改善UC大鼠的DAI和HI情况,其机制可能与抑制血小板的活化有关。
In order to explore the impact of Resina Draconis on platelet activation of ulcerative colitis(UC) rat model induced by dextran sulfate sodium(DSS) ,in this study 60 SD rats were randomly divided into five groups:groups A was blank control;group B, model control; group C, D, E were of treatment with Resina Draconis at low,middle,high dose respectively. Then the UC rat model was establised through DSS indu- cing;afterward,group A and B were given with normal saline(4 ml/a rat) gavage,meanwhile,group C,D, E with 600,1200 and 2400mg/kg(body weight) of Resina Draconis suspension in 4ml/a rat gavage, 1 time/ day,for 7 days continously. Followed by that after treatment DAI(disease activity index),and the expres- sion of platelet activation factor(PAF) and platelet factor 4(PF4) from plasma which was collected later 7 days after given drugs under anesthesia in above 5 groups were compared among five groups,as well as the histological injury (HI) status was observed following rats being sacrificed. As results,after treatment the DAI and HI score ratings of group C,D and E were significantly lower than that of groups B( P 〈0.05), but among group C,D and E there was no statistical differences( P 〉0.05) ;PAF and PF4 levels of group C,D and E were significantly lower than that of group B( P 〈0.05),but among group C,D and E there was no statistical differences( P 〉0.05) ;PAF and PF4 levels of group C,D and E were still higher than that of group A( P 〈0.05). Above results show that Resina Draconic can improve DAI and HI of UC rats at certain extent,its mechanism could be related to inhibiting platelet activation.
出处
《中国肛肠病杂志》
2013年第4期9-12,共4页
Chinese Journal of Coloproctology