中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2011年
2期
143-146
,共4页
丙戊酸钠%脂多糖%急性肺损伤%肿瘤坏死因子-α%白细胞介素-1β
丙戊痠鈉%脂多糖%急性肺損傷%腫瘤壞死因子-α%白細胞介素-1β
병무산납%지다당%급성폐손상%종류배사인자-α%백세포개소-1β
Valproic acid%Lipopolysaccharide%Acute lung injury%Tumor necrosis factor-alpha%Interleukin-1 belta
目的 研究丙戊酸钠(valproic acid,VPA)对脂多糖(lipopolysaccharide,LPS)诱导的大鼠急性肺损伤的影响.方法 实验地点在武汉协和医院中心实验室,通过股静脉注射LPS复制大鼠急性肺损伤模型,观察光镜下肺组织病理学改变、血清炎性因子和肺部炎性反应判定模型是否成功.依据干预药物的不同确定实验分组:股静脉给予5mL/kg生理盐水为对照组(NS组),股静脉给予LPS 10 mg/kg为模型组(LPS组),模型成功后股静脉给予VPA 300mg/kg治疗为治疗组(LPS+VPA组).注射LPS或NS后6 h处死动物,血气分析观察动脉血氧分压(PaO2)、肺泡气-动脉血氧分压差(A-aDO2)、乳酸(Lac),检测肺组织干湿重比(W/D),髓过氧化物酶(MPO)活性,肺泡灌洗液(BALF)中白蛋白质量浓度,用ELISA法检测6 h血清中TNF-α和IL-1β的含量,HE染色光镜下观察肺组织病理学变化.计量资料以均数±标准差(-x±s)表示,应用SPSS 13.0统计软件行单因素方差分析.结果 LPS组PaO2(mmHg)(81.50±3.24)较NS组(106.40±4.50)降低,A-aDO2(mmHg),Lac[(19.70±2.21),(3.63±0.22)]较NS组[(6.30±1.70),(1.21±0.19)]升高,W/D,MPO活性(μ/g),BALF中白蛋白质量浓度(pg/mL)分别为[(6.52±0.30),(7.25±0.49),(2.940±0.047)]较NS组[(4.38±0.17),(1.76±0.31),(0.099±0.077)]升高,血清中TNF-α和IL-1β的质量浓度(pg/ml)分别为(3325±284),(1950±222)较NS组(90±12),(50±11)显著升高,差异具有统计学意义(P＜0.05),LPS组肺组织出现病理学改变;与LPS组比较,LPS+VPA组上述指标除PaO2(mmHg)(94.50±4.38)上升外,其余指标均降至[(13.50±4.77),(2.13±1.02),(5.33±0.12),(4.38±0.42),(1.260±0.039),(2410±320),(1220±162)],差异具有统计学意义(P＜0.05),LPS+VPA组肺组织病理学改变明显减轻.结论 丙戊酸钠对脂多糖诱导的大鼠急性肺损伤有一定保护作用.
目的 研究丙戊痠鈉(valproic acid,VPA)對脂多糖(lipopolysaccharide,LPS)誘導的大鼠急性肺損傷的影響.方法 實驗地點在武漢協和醫院中心實驗室,通過股靜脈註射LPS複製大鼠急性肺損傷模型,觀察光鏡下肺組織病理學改變、血清炎性因子和肺部炎性反應判定模型是否成功.依據榦預藥物的不同確定實驗分組:股靜脈給予5mL/kg生理鹽水為對照組(NS組),股靜脈給予LPS 10 mg/kg為模型組(LPS組),模型成功後股靜脈給予VPA 300mg/kg治療為治療組(LPS+VPA組).註射LPS或NS後6 h處死動物,血氣分析觀察動脈血氧分壓(PaO2)、肺泡氣-動脈血氧分壓差(A-aDO2)、乳痠(Lac),檢測肺組織榦濕重比(W/D),髓過氧化物酶(MPO)活性,肺泡灌洗液(BALF)中白蛋白質量濃度,用ELISA法檢測6 h血清中TNF-α和IL-1β的含量,HE染色光鏡下觀察肺組織病理學變化.計量資料以均數±標準差(-x±s)錶示,應用SPSS 13.0統計軟件行單因素方差分析.結果 LPS組PaO2(mmHg)(81.50±3.24)較NS組(106.40±4.50)降低,A-aDO2(mmHg),Lac[(19.70±2.21),(3.63±0.22)]較NS組[(6.30±1.70),(1.21±0.19)]升高,W/D,MPO活性(μ/g),BALF中白蛋白質量濃度(pg/mL)分彆為[(6.52±0.30),(7.25±0.49),(2.940±0.047)]較NS組[(4.38±0.17),(1.76±0.31),(0.099±0.077)]升高,血清中TNF-α和IL-1β的質量濃度(pg/ml)分彆為(3325±284),(1950±222)較NS組(90±12),(50±11)顯著升高,差異具有統計學意義(P＜0.05),LPS組肺組織齣現病理學改變;與LPS組比較,LPS+VPA組上述指標除PaO2(mmHg)(94.50±4.38)上升外,其餘指標均降至[(13.50±4.77),(2.13±1.02),(5.33±0.12),(4.38±0.42),(1.260±0.039),(2410±320),(1220±162)],差異具有統計學意義(P＜0.05),LPS+VPA組肺組織病理學改變明顯減輕.結論 丙戊痠鈉對脂多糖誘導的大鼠急性肺損傷有一定保護作用.
목적 연구병무산납(valproic acid,VPA)대지다당(lipopolysaccharide,LPS)유도적대서급성폐손상적영향.방법 실험지점재무한협화의원중심실험실,통과고정맥주사LPS복제대서급성폐손상모형,관찰광경하폐조직병이학개변、혈청염성인자화폐부염성반응판정모형시부성공.의거간예약물적불동학정실험분조:고정맥급여5mL/kg생리염수위대조조(NS조),고정맥급여LPS 10 mg/kg위모형조(LPS조),모형성공후고정맥급여VPA 300mg/kg치료위치료조(LPS+VPA조).주사LPS혹NS후6 h처사동물,혈기분석관찰동맥혈양분압(PaO2)、폐포기-동맥혈양분압차(A-aDO2)、유산(Lac),검측폐조직간습중비(W/D),수과양화물매(MPO)활성,폐포관세액(BALF)중백단백질량농도,용ELISA법검측6 h혈청중TNF-α화IL-1β적함량,HE염색광경하관찰폐조직병이학변화.계량자료이균수±표준차(-x±s)표시,응용SPSS 13.0통계연건행단인소방차분석.결과 LPS조PaO2(mmHg)(81.50±3.24)교NS조(106.40±4.50)강저,A-aDO2(mmHg),Lac[(19.70±2.21),(3.63±0.22)]교NS조[(6.30±1.70),(1.21±0.19)]승고,W/D,MPO활성(μ/g),BALF중백단백질량농도(pg/mL)분별위[(6.52±0.30),(7.25±0.49),(2.940±0.047)]교NS조[(4.38±0.17),(1.76±0.31),(0.099±0.077)]승고,혈청중TNF-α화IL-1β적질량농도(pg/ml)분별위(3325±284),(1950±222)교NS조(90±12),(50±11)현저승고,차이구유통계학의의(P＜0.05),LPS조폐조직출현병이학개변;여LPS조비교,LPS+VPA조상술지표제PaO2(mmHg)(94.50±4.38)상승외,기여지표균강지[(13.50±4.77),(2.13±1.02),(5.33±0.12),(4.38±0.42),(1.260±0.039),(2410±320),(1220±162)],차이구유통계학의의(P＜0.05),LPS+VPA조폐조직병이학개변명현감경.결론 병무산납대지다당유도적대서급성폐손상유일정보호작용.
Objective To investigate the effects of valproic acid (VPA) on acute lung injury induced by Lipopolysaccharide in rats. Method The rat model of acute lung injury was made by intravenous injection of lipopolysaccharide (LPS). The pathological changes of lung were observed under light microscope and inflammatory cytokines in serum detected by using ELISA to judge whether the model was successfully done or not. All rats were divided into three groups as per the different intervention agents employed. Rats in control group were treated with intravenous injection of NS in dose of 5 ml/kg, rats in LPS group were exposed to LPS with dosage of 10 mg/kg and model rats in LPS + VPA group were treated with VPA in dose of 300 mg/kg. The rats were sacrificed 6 h after LPS or NS administration. The blood PaO2 ,A-aDO2 and blood lactic acid (Lac) were measured, the lungs were removed for observing the histopathological changes and determination of wet/dry lung weight (W/D) ratio and myeloperoxidase (MPO) activity as well as albumin concentration in broncho-alveolar lavage fluid (BALF) . Seurm was collected to determine the concentrations of tumor necrosis factor-a (TNF-α) and interleukin-1β( IL-1 β) by using LISA 6 h later. All data were presented in ((x)±s). One-way ANOVA was used for comparing differences between groups. Results Compared with acute lung injury group, the blood PaO2 (94. 50 ± 4.38 ) in rats of LPS + VPA group was higher, whereas A-aDO2 ( 13.50 ± 4.77 ) and blood lac( 2.13 ± 1. 02 ) in LPS + VPA group were lower. VPA significantly lowered W/D (5.33 ±0. 12) ratio and MPO activity (4.38 ±0. 42) in the lung. Albumin concentration ( 1. 260 ± 0. 039 ) in BALF, and the levels of TN F-α( 2 410 ±320 )and IL-1β( 1 220 ± 162 )in serum were lower in LPS + VPA group. The histological changes of lung injury were lessened by VPA. Conclusions Valproic acid has protective effects against lipopolysaccharide-induced acute lung injury in rats.
