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机构地区:[1]浙江中医药大学附属第一医院消化科,杭州310006
出 处:《医药导报》2009年第9期1127-1130,共4页Herald of Medicine
摘 要:目的利用短期小剂量双氯芬酸灌胃,诱导小肠黏膜损伤,建立大鼠非甾体类抗炎药(NSAIDs)肠黏膜损伤模型,观察云母对NSAIDs所致小肠黏膜损伤的预防作用,为防治该损伤提供实验依据。方法设立空白组、模型组、云母组,每组16只大鼠,再随机分为急性期(T1)、亚急性期(T2)亚组,每小组8只。云母组:空白组以纯化水1 mL灌胃,bid;模型组以双氯芬酸7.5 mg.kg-1灌胃,bid;云母组提前1 d以云母60 mg.kg-1灌胃1次,之后以双氯芬酸7.5 mg.kg-1加上云母60 mg.kg-1灌胃,bid,T1亚组灌胃1 d后处死,T2亚组灌胃5 d后处死。检测大鼠血清一氧化氮含量,观察小肠损伤程度。结果小剂量双氯芬酸能引起小肠黏膜显著出血性损伤,小肠黏膜可见大量红斑、糜烂、溃疡,局部肠腔可见囊样扩张。T1、T2模型组损伤均大于空白组(均P<0.05),模型组T2亚组损伤明显大于模型组T1亚组(P<0.05)。云母组损伤均小于模型组(均P<0.05)。模型组T1亚组血清一氧化氮含量明显小于空白组(P<0.05),模型组T2亚组血清一氧化氮含量明显大于空白组(P<0.05);模型组与云母组的T1、T2亚组之间一氧化氮含量比较差异无显著性(均P>0.05)。结论短期小剂量双氯芬酸灌胃可引起小肠黏膜损伤,并随时间呈进行性加重;血清一氧化氮含量在小肠黏膜损伤后呈现先降低、后升高的趋势。云母对NSAIDs诱发的小肠黏膜损伤具有一定的预防作用,其保护作用可能并不依赖一氧化氮途径。Objective To set up the small intestinal mucosal damage model by short-term administration of diclofenac at low dose. And to investigate the preventive effect of mica on NSAIDs induced small intestinal damage, providing the experimental foundation for preventing and controlling this damage. Methods Forty-eight rats were divided into 3 groups (control group, model group and mica group), and each group with 16 rats were separated into T1 (acute stage), T2 (subacute stage) subgroups. Rats in the mica group were lavaged with mica (60 mg · kg-1) 1 day beforehand, and then with both mica 60 mg· kg-1and diclofenac 7.5 mg · kg-1 , bid ; rats in the control group were treated with 1 mL distilled water, bid ; in the model group treated with diclofenae 7.5 mg · kg-1, bid. The Tl and T2 group were killed in 1 d and 5 d later,respectively. Results A single administration of low-dose diclofenac induced multiple lesions in the small intestine, such as obviously erythema, erosion, ulcer and cystoid expansion. The lesions of the model T2 subgroup was more seriously than those in the T1 subgroup (P 〈 0.05 ). And the lesions in the model group was also more obviously than those in the control and mica group (both T~ and T2, P 〈 0. 05). Compared with the control group, the serum content of NO in the model TI subgroup was significantly lower ( P 〈 0.05 ), while that in T2 subgroup was higher ( P 〈 0.05 ) ; no difference was found among the mica group and model groups ( each P 〉 0.05 ). Conclusion Short term administration of low-dose diclofenac elicites intestinal mueosal lesions and aggravates as time goes on. The NO content in serum presents a tendency with decrease at first but increase later. The mica has certain preventive effect on small intestinal lesions ,which maybe not rely on the NO pathway.
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