天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2009年
7期
538-540
,共3页
温学红%张虹%李海英%李月川%孙增涛
溫學紅%張虹%李海英%李月川%孫增濤
온학홍%장홍%리해영%리월천%손증도
抗肿瘤药%顺铂%胸水%纤溶酶原激活物抑制物1%转化生长因子β%肿瘤坏死因子α
抗腫瘤藥%順鉑%胸水%纖溶酶原激活物抑製物1%轉化生長因子β%腫瘤壞死因子α
항종류약%순박%흉수%섬용매원격활물억제물1%전화생장인자β%종류배사인자α
antineoplastic agents%cisplatin%hydrothorax%plasminogen activator inhibitor 1%transforming growth factor beta%tumor necrosis factor-alpha
目的:观察康莱特联合顺铂胸腔注入前后I型纤溶酶原激活物抑制剂(PAI-1)、转化生长因子13(TGF-β)、肿瘤坏死因子α(TNF-α)指标的变化,为明确其发生作用机制提供实验理论.方法:将患者随机分为联合用药组、康莱特组和顺铂组,在胸腔注药前及注药24、48 h后取胸水标本,采用酶联免疫方法测定胸水中PAI-1、TGF-β和TNF-α的含量.结果:3组在注药24、48h后PAI-1、TGF-B、TNF-α含量均比治疗前升高,差别有统计学意义(P<0.05).注药24 h后PAI-1、TGF-β水平在3组间比较差别无统计学意义,而TNF-α在联合组要高于康莱特组和顺铂组,差别有统计学意义(P<0.05).注药48 h后PAI-1、TGF-β、TNF-α含量在联合组要高于康莱特组,差别有统计学意义(P<0.05).结论:康莱特和顺铂联合用药后激活PAI-1、TGF-13、TNF-α等细胞因子,产生炎症反应并抑制纤溶活性,促进纤维蛋白生成和沉积并诱导胸膜粘连,其作用效果要优于单纯用康莱特或顺铂.
目的:觀察康萊特聯閤順鉑胸腔註入前後I型纖溶酶原激活物抑製劑(PAI-1)、轉化生長因子13(TGF-β)、腫瘤壞死因子α(TNF-α)指標的變化,為明確其髮生作用機製提供實驗理論.方法:將患者隨機分為聯閤用藥組、康萊特組和順鉑組,在胸腔註藥前及註藥24、48 h後取胸水標本,採用酶聯免疫方法測定胸水中PAI-1、TGF-β和TNF-α的含量.結果:3組在註藥24、48h後PAI-1、TGF-B、TNF-α含量均比治療前升高,差彆有統計學意義(P<0.05).註藥24 h後PAI-1、TGF-β水平在3組間比較差彆無統計學意義,而TNF-α在聯閤組要高于康萊特組和順鉑組,差彆有統計學意義(P<0.05).註藥48 h後PAI-1、TGF-β、TNF-α含量在聯閤組要高于康萊特組,差彆有統計學意義(P<0.05).結論:康萊特和順鉑聯閤用藥後激活PAI-1、TGF-13、TNF-α等細胞因子,產生炎癥反應併抑製纖溶活性,促進纖維蛋白生成和沉積併誘導胸膜粘連,其作用效果要優于單純用康萊特或順鉑.
목적:관찰강래특연합순박흉강주입전후I형섬용매원격활물억제제(PAI-1)、전화생장인자13(TGF-β)、종류배사인자α(TNF-α)지표적변화,위명학기발생작용궤제제공실험이론.방법:장환자수궤분위연합용약조、강래특조화순박조,재흉강주약전급주약24、48 h후취흉수표본,채용매련면역방법측정흉수중PAI-1、TGF-β화TNF-α적함량.결과:3조재주약24、48h후PAI-1、TGF-B、TNF-α함량균비치료전승고,차별유통계학의의(P<0.05).주약24 h후PAI-1、TGF-β수평재3조간비교차별무통계학의의,이TNF-α재연합조요고우강래특조화순박조,차별유통계학의의(P<0.05).주약48 h후PAI-1、TGF-β、TNF-α함량재연합조요고우강래특조,차별유통계학의의(P<0.05).결론:강래특화순박연합용약후격활PAI-1、TGF-13、TNF-α등세포인자,산생염증반응병억제섬용활성,촉진섬유단백생성화침적병유도흉막점련,기작용효과요우우단순용강래특혹순박.
Objective: To detect the levels of plasminogen activator inhibitor-I (PAI-1), transforming growth factor-β (TGF-β)and tumor necrosis factor-α (TNF-α) in the pleural fluid before and after intrapleural injection of Kanglaite combined with Cisplatin, and the mechanisms thereof. Methods: Patients were randomly divided into three groups, the Kanglaite combined with Cisplatin group (combination treatment group), Kangkaite group and Cisplatin group. The levels of PAl-1, TGF-β and TNF-α were determined by ELISA in pleural effusion 24 h and 48 h before and after intrapleural injection of medicine. Results: The levels of PAI-1, TGF-βand TNF-αawere higher 24 h and 48 h after treatment compared with those of pre-treatment in three groups (P<0.05). There were no statistical significances in levels of PAI-1 and TGF-β24 h after injection medicine in three groups. But the level of TNF-α was higher in the combination treatment group than that in Kangkaite and Cisplatin groups(P<0.05). After injection medicine 48 h, the levels of PAl-I, GF-β and TNF-α were higher in the combination treatment group than those in Kangkaite group (P<0.05). Conclusion: The treatment of Kanglaite combined with Cisplatin activates PAI-1, TGF-β and TNF-αcytokines and causes inflammatory, suppresses fibrinolytic activity. These cytokines promote fibrin and induce pleural adhesion.