CAJ | 학술논문

目的研究有机磷农药敌敌畏中毒后小鼠肠黏膜屏障功能的变化及新型抗毒剂宾赛克嗪的保护作用.方法昆明小鼠65只,雌雄各半,随机分为正常对照组、敌敌畏染毒模型组、宾赛克嗪2,6,18mg/ks预防治疗组;各预防治疗组腹腔注射预防给予相应约物,10min后灌胃给予敌敌畏55mg/ks,于染毒后3 h取血,使用紫外分光光度计检测血浆二胺氧化酶(DAO)活性及D-乳酸质量浓度,采用单因素方差分析定量数据.结果与正常对照组比较,模型组血浆DAO活性明显升高(P<0.01);与模型组比较,各预防治疗组血浆DAO活性明显下降(P<0.01),其中6 mg/kg预防治疗组效果最好;与正常对照组比较,模型组血浆D-乳酸质量浓度明显升高(P<0.01);与模型组比较,各预防治疗组血浆D-酸质量浓度叫显降低(P<0.01),并且能呈剂量依赖性降低D-酸质量浓度.结论敌敌畏染毒小鼠血浆DAO活性及D-酸质量浓度显著增高,肠黏膜屏障功能遭到破坏,宾赛克嗪能减轻肠黏膜屏障功能的损伤,具有保护作用.
목적 연구유궤린농약활활외중독후소서장점막병장공능적변화급신형항독제빈새극진적보호작용.방법곤명소서65지,자웅각반,수궤분위정상대조조、활활외염독모형조、빈새극진2,6,18mg/ks예방치료조;각예방치료조복강주사예방급여상응약물,10min후관위급여활활외55mg/ks,우염독후3 h취혈,사용자외분광광도계검측혈장이알양화매(DAO)활성급D-유산질량농도,채용단인소방차분석정량수거.결과 여정상대조조비교,모형조혈장DAO활성명현승고(P<0.01);여모형조비교,각예방치료조혈장DAO활성명현하강(P<0.01),기중6 mg/kg예방치료조효과최호;여정상대조조비교,모형조혈장D-유산질량농도명현승고(P<0.01);여모형조비교,각예방치료조혈장D-산질량농도규현강저(P<0.01),병차능정제량의뢰성강저D-산질량농도.결론 활활외염독소서혈장DAO활성급D-산질량농도현저증고,장점막병장공능조도파배,빈새극진능감경장점막병장공능적손상,구유보호작용.
Objective To investigate the change of gut-barrier function of mice in acute organophosphorus poisoning and the protection effect of benthiactzine. Method A total of 65 Kunming mice, female and male both half, were randomly assigned to five groups: normal group, DDVP poisoning(model) group, and benthiactzine 2, sured by spectrophotometric assay at 3 hours after DDVP poisoning. The variance analysis was used to deal the quantitative data. Results The DAO activity in model group significantly increased compared with normal group (P < 0.01). Whereas, the DAO activity in all pretreatment groups were significantly decreased compared with concentration of D-lactate in model group was significantly increased compared with normal group (P < 0.01). However, the concentration of D-lactate in pretreatment groups was significantly decreased compared with model group(all P < 0.01). The concentration of D-lactate could be decreased dose-dependently by the administration of benthiactzine. Conclusions The diamine oxidase activity and concentration of D-lactate were significantly in-creased in the DDVP poisoning mice, which means the gnt-barrier function was severely damaged. And the admin-istration of benthiactzine could alleviate the injury to the gut-barrier function.