中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2012年
6期
457-459
,共3页
周从阳%谢姝%罗雅娟%汤旭惠%李凡
週從暘%謝姝%囉雅娟%湯旭惠%李凡
주종양%사주%라아연%탕욱혜%리범
百草枯%乌司他丁%4-羟基壬烯醛%大鼠
百草枯%烏司他丁%4-羥基壬烯醛%大鼠
백초고%오사타정%4-간기임희철%대서
Paraquat%Ulinastatin%4-hydroxynonenal%Rats
目的 观察乌司他丁(UTI)对百草枯(PQ)中毒大鼠肺组织中4-羟基壬烯醛(4-HNE)表达的影响.方法 将72只SD大鼠按随机数字表法分为对照组、染毒组、UTI干预组,每组24只.染毒组、UTI干预组PQ灌胃(80 mg/kg)染毒建立SD大鼠肺损伤模型;对照组组等量生理盐水灌胃.UTI干预组于PQ灌胃后30 min腹腔内注射UTI 10万U/kg;对照组、染毒组腹腔注射等量生理盐水.不同处理后12、24、48、72 h观察3组大鼠肺组织病理改变及检测肺组织中4HNE表达.结果 染毒后12h,染毒组和UTI干预组大鼠肺组织4-HNE表达升高,48h达高峰,72 h 4-HNE表达下降,但仍较高.与对照组组比较,染毒组和干预组大鼠肺组织4-HNE表达明显升高,差异有统计意义(P＜0.05).干预组大鼠肺组织4-HNE表达明显低于染毒组,差异有统计意义(P＜0.01).肺组织病理学观察可见,对照组无明显变化;染毒组、干预组肺泡毛细血管扩张,伴弥漫性肺出血,肺泡腔塌陷,肺泡腔内炎性细胞浸润,其中干预组较染毒组为轻.结论 PQ中毒时4-HNE表达增强;UTI能减少4-HNE的产生,减轻PQ中毒大鼠的肺损伤.
目的 觀察烏司他丁(UTI)對百草枯(PQ)中毒大鼠肺組織中4-羥基壬烯醛(4-HNE)錶達的影響.方法 將72隻SD大鼠按隨機數字錶法分為對照組、染毒組、UTI榦預組,每組24隻.染毒組、UTI榦預組PQ灌胃(80 mg/kg)染毒建立SD大鼠肺損傷模型;對照組組等量生理鹽水灌胃.UTI榦預組于PQ灌胃後30 min腹腔內註射UTI 10萬U/kg;對照組、染毒組腹腔註射等量生理鹽水.不同處理後12、24、48、72 h觀察3組大鼠肺組織病理改變及檢測肺組織中4HNE錶達.結果 染毒後12h,染毒組和UTI榦預組大鼠肺組織4-HNE錶達升高,48h達高峰,72 h 4-HNE錶達下降,但仍較高.與對照組組比較,染毒組和榦預組大鼠肺組織4-HNE錶達明顯升高,差異有統計意義(P＜0.05).榦預組大鼠肺組織4-HNE錶達明顯低于染毒組,差異有統計意義(P＜0.01).肺組織病理學觀察可見,對照組無明顯變化;染毒組、榦預組肺泡毛細血管擴張,伴瀰漫性肺齣血,肺泡腔塌陷,肺泡腔內炎性細胞浸潤,其中榦預組較染毒組為輕.結論 PQ中毒時4-HNE錶達增彊;UTI能減少4-HNE的產生,減輕PQ中毒大鼠的肺損傷.
목적 관찰오사타정(UTI)대백초고(PQ)중독대서폐조직중4-간기임희철(4-HNE)표체적영향.방법 장72지SD대서안수궤수자표법분위대조조、염독조、UTI간예조,매조24지.염독조、UTI간예조PQ관위(80 mg/kg)염독건립SD대서폐손상모형;대조조조등량생리염수관위.UTI간예조우PQ관위후30 min복강내주사UTI 10만U/kg;대조조、염독조복강주사등량생리염수.불동처리후12、24、48、72 h관찰3조대서폐조직병리개변급검측폐조직중4HNE표체.결과 염독후12h,염독조화UTI간예조대서폐조직4-HNE표체승고,48h체고봉,72 h 4-HNE표체하강,단잉교고.여대조조조비교,염독조화간예조대서폐조직4-HNE표체명현승고,차이유통계의의(P＜0.05).간예조대서폐조직4-HNE표체명현저우염독조,차이유통계의의(P＜0.01).폐조직병이학관찰가견,대조조무명현변화;염독조、간예조폐포모세혈관확장,반미만성폐출혈,폐포강탑함,폐포강내염성세포침윤,기중간예조교염독조위경.결론 PQ중독시4-HNE표체증강;UTI능감소4-HNE적산생,감경PQ중독대서적폐손상.
Objective To investigate the 4-hydroxynonenal (4-HNE) expression changes and the impact of ulinastatin (UTI).Methods Seventy-two healthy Sprague-Dawley rats were randomly divided into three groups:the control group,poisoning group and treatment group,with 24 rats in each group.The model of lung injury was established by intragastric PQ (80 mg/kg) administration in poisoning group and treatment group,and 1 mL saline was administered intragastrically in the control group.The rats in treatmeut group were injected intraperitoneally with UTI (100 000 U/kg) 30 minutes after PQ administration,and the rats in the control group and poisoning group were intraperitoneally injected with the same volume of saline.After different treatments,the pathological changes and the expression of 4-HNE in lung tissue was detected in 12,24,and 72 h in three groups.Results In the poisoning group and treatment group,the expression of 4-HNE in lung tissue of rats were increased in 12 h after poisoning and reached the peak in 48 h; in 72 h after poisoning,the expression of 4-HNE in lung tissue were decreased,but they were still high.Compared with the control group,the expression of 4-HNE in lung tissue of rats were significantly increased in the poisoning group and treatment group (P＜0.05).And compared with the poisoning group,the expression of 4-HNE in lung tissue of rats were significantly decreased in the treatment group (P＜0.01).The pathological changes were observed,including alveolar capillary expansion,diffuse alveolar hemorrhage and alveolar inflammation cell infiltration,were found in lungs of rats in poisoning group and treatment group.There is no significant change in the control group.Compared with the control group,the expression of 4-HNE in lung tissue significantly increased in poisoning group and treatment group (P＜0.01),but the expression in treatment group was lower than in poisoning group (P＜0.01).Conclusion The expression of 4-HNE increased in PQ intoxicated rats.UTI may reduce the expression of 4-HNE and reduce lung injury in PQ intoxicated rats.
