实用药物与临床
實用藥物與臨床
실용약물여림상
Practical Pharmacy and Clinical Remedies
2015年
11期
1305-1309
,共5页
申严%卓宋明%庄虹%李娜%余海彬
申嚴%卓宋明%莊虹%李娜%餘海彬
신엄%탁송명%장홍%리나%여해빈
急性肺损伤%脂多糖%尤文%地塞米松%炎症因子
急性肺損傷%脂多糖%尤文%地塞米鬆%炎癥因子
급성폐손상%지다당%우문%지새미송%염증인자
Acute lung injury%Lipopolysaccharide%Omeganven%Dexamethasone%Inflammatory factor
目的 明确尤文联合地塞米松对大鼠急性肺损伤模型的效果及其相关机制. 方法 将96 只SD大鼠分别于气管内滴注LPS制备急性肺损伤模型,随机分为溶媒对照组( LPS组)、英脱利匹特组(ω-6 组)、尤文组(ω-3组)、地塞米松组( DXM组)、英脱利匹特+地塞米松组(ω-6 +DXM组)、尤文+地塞米松组(ω-3 +DXM组) ,分别给予相应的干预处理3 d后,HE染色检测肺组织病理改变,测定PaO2 及肺组织湿/干重比( W/D) ,ELISA法检测BALF中相关炎症因子的含量. 结果 LPS组与ω-6组大鼠肺泡隔增厚,肺组织出血、水肿及大量炎性细胞浸润,肺组织W/D比值明显高于其他各组;给予地塞米松或尤文后,模型大鼠死亡率降低,肺损伤程度减轻,PaO2 升高,BALF中TNF-α、IL-1β、IL-6含量降低( P<0. 05 ). ω-3 组、DXM组、ω-6 +DXM组之间各检测指标无明显区别,而ω-3+DXM组肺组织基本正常,W/D比值最低,PaO2 最高,BALF中TNF-α、IL-1β、IL-6含量明显低于其他各组;给予尤文后BALF中IL-10 明显增高,ω-3 组与ω-3 +DXM组BALF中IL-10 明显高于其他各组,差异均有统计学意义( P<0. 05 ). 结论 尤文联合地塞米松可通过调控TNF-α、IL-1β、IL-6 及IL-10等相关炎症因子的表达,减轻肺损伤.
目的 明確尤文聯閤地塞米鬆對大鼠急性肺損傷模型的效果及其相關機製. 方法 將96 隻SD大鼠分彆于氣管內滴註LPS製備急性肺損傷模型,隨機分為溶媒對照組( LPS組)、英脫利匹特組(ω-6 組)、尤文組(ω-3組)、地塞米鬆組( DXM組)、英脫利匹特+地塞米鬆組(ω-6 +DXM組)、尤文+地塞米鬆組(ω-3 +DXM組) ,分彆給予相應的榦預處理3 d後,HE染色檢測肺組織病理改變,測定PaO2 及肺組織濕/榦重比( W/D) ,ELISA法檢測BALF中相關炎癥因子的含量. 結果 LPS組與ω-6組大鼠肺泡隔增厚,肺組織齣血、水腫及大量炎性細胞浸潤,肺組織W/D比值明顯高于其他各組;給予地塞米鬆或尤文後,模型大鼠死亡率降低,肺損傷程度減輕,PaO2 升高,BALF中TNF-α、IL-1β、IL-6含量降低( P<0. 05 ). ω-3 組、DXM組、ω-6 +DXM組之間各檢測指標無明顯區彆,而ω-3+DXM組肺組織基本正常,W/D比值最低,PaO2 最高,BALF中TNF-α、IL-1β、IL-6含量明顯低于其他各組;給予尤文後BALF中IL-10 明顯增高,ω-3 組與ω-3 +DXM組BALF中IL-10 明顯高于其他各組,差異均有統計學意義( P<0. 05 ). 結論 尤文聯閤地塞米鬆可通過調控TNF-α、IL-1β、IL-6 及IL-10等相關炎癥因子的錶達,減輕肺損傷.
목적 명학우문연합지새미송대대서급성폐손상모형적효과급기상관궤제. 방법 장96 지SD대서분별우기관내적주LPS제비급성폐손상모형,수궤분위용매대조조( LPS조)、영탈리필특조(ω-6 조)、우문조(ω-3조)、지새미송조( DXM조)、영탈리필특+지새미송조(ω-6 +DXM조)、우문+지새미송조(ω-3 +DXM조) ,분별급여상응적간예처리3 d후,HE염색검측폐조직병리개변,측정PaO2 급폐조직습/간중비( W/D) ,ELISA법검측BALF중상관염증인자적함량. 결과 LPS조여ω-6조대서폐포격증후,폐조직출혈、수종급대량염성세포침윤,폐조직W/D비치명현고우기타각조;급여지새미송혹우문후,모형대서사망솔강저,폐손상정도감경,PaO2 승고,BALF중TNF-α、IL-1β、IL-6함량강저( P<0. 05 ). ω-3 조、DXM조、ω-6 +DXM조지간각검측지표무명현구별,이ω-3+DXM조폐조직기본정상,W/D비치최저,PaO2 최고,BALF중TNF-α、IL-1β、IL-6함량명현저우기타각조;급여우문후BALF중IL-10 명현증고,ω-3 조여ω-3 +DXM조BALF중IL-10 명현고우기타각조,차이균유통계학의의( P<0. 05 ). 결론 우문연합지새미송가통과조공TNF-α、IL-1β、IL-6 급IL-10등상관염증인자적표체,감경폐손상.
Objective To explore the effects of omeganven combined with dexamethasone on the acute lung injury of rat model and the mechanism. Methods Ninety-six SD rats were treated with lipopolysaccharide ( LPS) by intratracheal instillation to induce acute lung injury,and they were randomly divided into control group ( LPS group) , intralipid group (ω-6 group) ,omeganven group (ω-3 group) ,dexamethasone group ( DXM group) ,intralipid+dexa-methasone group (ω-6+DXM group) and omeganven+dexamethasone group (ω-3+DXM group). After 3 d of cor-responding treatment,the pathologic changes in lung tissue section,wet/dry weight ratio (W/D) of lung tissue and PaO2 were measured. The concentration of TNF-α, IL-1β, IL-6 and IL-10 in broncho-alveolar lavage fluid ( BALF ) were respectively measured by ELISA. Results In rats of LPS group and ω-6 group,alveolar septum thickening,lung hemorrhage,edema and inflammatory cell infiltration in lung tissue were easily seen,and W/D ratio of lung tissue was significantly higher than that of another groups. Among rats of ω-3 group,DXM group and ω-6 +DXM group,there was no obvious difference in pathological changes,and the level of TNF-α,IL-1βand IL-6 in BALF,however,the inde-xes decreased significantly after treatment in DXM group and ω-3 group. In rats of ω-3+DXM group,the structure of lung tissue was almost normal,and the W/D ratio and the levels of TNF-α,IL-1β and IL-6 in BALF were the lowest (P<0. 05). Furthermore,the level of IL-10 in BALF increased remarkably after treatment with omeganven,and it was obviously higher in rats of ω-3 group and ω-3 +DXM group ( P <0. 05 ) . Conclusion Omeganven combined with dexamethasone can relieve lung injury through regulating the expression of inflammatory factor in BALF such as TNF-α,IL-1β,IL-6 and IL-10 in rats with acute lung injury.
