中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2012年
6期
437-440
,共4页
史晶%高渝峰%陈少波%潘启豪%廖晓星%胡春林
史晶%高渝峰%陳少波%潘啟豪%廖曉星%鬍春林
사정%고투봉%진소파%반계호%료효성%호춘림
百草枯%呼吸窘迫综合征,成人%NF-κB%吡咯烷二硫代氨基甲酸
百草枯%呼吸窘迫綜閤徵,成人%NF-κB%吡咯烷二硫代氨基甲痠
백초고%호흡군박종합정,성인%NF-κB%필각완이류대안기갑산
Paraquat%Respiratory distress syndrome,adult%NF-kappa B%Pyrrolidine dithiocarbamate
目的 观察核因子(NF)-κB抑制剂吡咯烷二硫代氨基甲酸(PDTC)对百草枯(PQ)中毒后早期肺损伤的影响.方法 64只成年雄性SD大鼠建立PQ肺损伤模型,数字随机法分为PQ+PDTC和PQ+PBS组,每组32只.PQ+PDTC组给予PDTC 100 mg/kg腹腔内注射,PQ+PBS组给予PBS腹腔内注射.24、48和72 h后观察两组动物存活率,应用苏木精-伊红(HE)染色观察急性肺损伤(ALL)情况并评分；免疫组化检测肺组织炎性细胞浸润；ELISA法检测肺组织内TNF-α、IL-6含量和免疫印迹法检测肺内NF-κB激活情况.结果 与PQ+PBS组相比,PDTC提高大鼠PQ中毒后的72 h内存活率[24/32(75％)比13/32(40.6％),P=0.015].PDTC改善大鼠PQ中毒后24、48 h和72 h的肺损伤评分(7.5±1.0比9.8±1.5,9.7±0.8比12.0±0.9,11.5±1.0比14.5±1.0,均P＜0.05).PDTC降低大鼠PQ中毒后24、48 h和72 h的肺内髓过氧化物酶(MPO)阳性细胞数、肺组织内TNF-α、IL-6蛋白水平和胞核、胞质NF-κB P65蛋白浓度(均P＜0.05).结论 PDTC可减少大鼠PQ中毒后早期炎性细胞的浸润并抑制NF-κB的激活,使致炎因子TNF-α、IL-6表达下降,减轻肺损伤,降低早期病死率.
目的 觀察覈因子(NF)-κB抑製劑吡咯烷二硫代氨基甲痠(PDTC)對百草枯(PQ)中毒後早期肺損傷的影響.方法 64隻成年雄性SD大鼠建立PQ肺損傷模型,數字隨機法分為PQ+PDTC和PQ+PBS組,每組32隻.PQ+PDTC組給予PDTC 100 mg/kg腹腔內註射,PQ+PBS組給予PBS腹腔內註射.24、48和72 h後觀察兩組動物存活率,應用囌木精-伊紅(HE)染色觀察急性肺損傷(ALL)情況併評分；免疫組化檢測肺組織炎性細胞浸潤；ELISA法檢測肺組織內TNF-α、IL-6含量和免疫印跡法檢測肺內NF-κB激活情況.結果 與PQ+PBS組相比,PDTC提高大鼠PQ中毒後的72 h內存活率[24/32(75％)比13/32(40.6％),P=0.015].PDTC改善大鼠PQ中毒後24、48 h和72 h的肺損傷評分(7.5±1.0比9.8±1.5,9.7±0.8比12.0±0.9,11.5±1.0比14.5±1.0,均P＜0.05).PDTC降低大鼠PQ中毒後24、48 h和72 h的肺內髓過氧化物酶(MPO)暘性細胞數、肺組織內TNF-α、IL-6蛋白水平和胞覈、胞質NF-κB P65蛋白濃度(均P＜0.05).結論 PDTC可減少大鼠PQ中毒後早期炎性細胞的浸潤併抑製NF-κB的激活,使緻炎因子TNF-α、IL-6錶達下降,減輕肺損傷,降低早期病死率.
목적 관찰핵인자(NF)-κB억제제필각완이류대안기갑산(PDTC)대백초고(PQ)중독후조기폐손상적영향.방법 64지성년웅성SD대서건립PQ폐손상모형,수자수궤법분위PQ+PDTC화PQ+PBS조,매조32지.PQ+PDTC조급여PDTC 100 mg/kg복강내주사,PQ+PBS조급여PBS복강내주사.24、48화72 h후관찰량조동물존활솔,응용소목정-이홍(HE)염색관찰급성폐손상(ALL)정황병평분；면역조화검측폐조직염성세포침윤；ELISA법검측폐조직내TNF-α、IL-6함량화면역인적법검측폐내NF-κB격활정황.결과 여PQ+PBS조상비,PDTC제고대서PQ중독후적72 h내존활솔[24/32(75％)비13/32(40.6％),P=0.015].PDTC개선대서PQ중독후24、48 h화72 h적폐손상평분(7.5±1.0비9.8±1.5,9.7±0.8비12.0±0.9,11.5±1.0비14.5±1.0,균P＜0.05).PDTC강저대서PQ중독후24、48 h화72 h적폐내수과양화물매(MPO)양성세포수、폐조직내TNF-α、IL-6단백수평화포핵、포질NF-κB P65단백농도(균P＜0.05).결론 PDTC가감소대서PQ중독후조기염성세포적침윤병억제NF-κB적격활,사치염인자TNF-α、IL-6표체하강,감경폐손상,강저조기병사솔.
Objective To determine the effects of pyrrolidine dithiocarbamate(PDTC),a nuclear factor-κB (NF-κB) inhibitor,on paraquat-induced early-stage acute lung injury.Methods Following establishment of paraquat-induced lung injury mice model,64 adult male SD rats were randomly divided into PQ+PBS gioup (32 SD rats were treated with phosphate buffer solution) and PQ+PDTC group (32 SD rats were treatecl with 100 mg/kg PDTC).The survival rate of two groups was assessed at hours 24,48 and 72 respectively.Haematoxylin-eosin staining was employed to assess the acute lung injury for scoring,and immunochemical assay was used to detect inflammatory cell infiltration in the lungs.The level of TNF-α and IL-6 was measured by enzyme-linked immunosorbent assay and activation of NF-κB in the lungs was assessed by using Western blotting.Results PDTC improved the survival rate at 72 hours as compared with group PQ+PBS[24/32(75％) in group PQ+PDTC vs 13/32(40.6%) in group PQ+PBS,P=0.015] and acute lung injury score at 24 hours (7.5±1.0 vs 9.8±1.5),48 hours (9.7±0.8 vs 12.0±0.9) and 72 hours (11.5±1.0 vs 14.5±1.0) (all P＜0.05).PDTC resulted in reduced cell count with myeloperoxidase expression,the levels of TNF-α and IL-6 in the lungs and the protein levels of NF-κB in the nucleus and cytoplasm (all P＜0.05).Conclusion PDTC reduces early-stage mortality of acute lung injury by suppressing infiltration of myeloperoxidase-positive inflammatory cells and inhibiting NF-κB activation leading to decreased TNF-α and IL-6 expression in the lungs.
