姜黄素对肠炎大鼠肠黏膜基质金属蛋白酶-9的调控

目的:探索姜黄素对炎症性肠病(IBD)模型大鼠肠黏膜炎症靶点基质金属蛋白酶(MMP)-9的影响.方法:建立以三硝基苯磺酸诱导的大鼠IBD模型.模型大鼠给予含20g/L姜黄素的饲料喂养,药物对照组给予含2 g/L N-乙酰半胱氨酸和5g/L柳氮磺胺吡啶的饲料喂养,模型组及正常对照组给予普通饲料喂养.评价肠炎大鼠死亡率及肠黏膜病理组织学评分.电泳迁移率改变分析法检测肠黏膜胞核NF-κB活性的变化.应用Western印迹分析法检测肠黏膜细胞质IκB.半定量RT-PCR检测MMP-9 mRNA的表达.结果:姜黄素可降低IBD模型大鼠死亡率及改善肠黏膜病理组织学症状.姜黄素可抑制IBD模型大鼠肠黏膜胞质IκB的降解并抑制胞核NF-κB的激活,同时降低MMP-9的表达.结论:姜黄素可预防和改善IBD鼠科模型中的实验性肠炎,调控MMP-9的表达;MMP-9可作为观察抗肠炎药物药效的指标之一,姜黄素对治疗IBD有应用前景.     

姜黄素对肠炎大鼠肠黏膜环氧合酶-2的调控

目的: 探索姜黄素对炎症性肠病(IBD)模型大鼠肠黏膜炎症靶点环氧合酶-2(COX-2)的影响.方法: 建立以三硝基苯磺酸(TNBS)诱导的大鼠肠炎模型.模型大鼠给予含20 g/L的姜黄素饲料喂养,药物阳性对照组给予含5 g/L柳氮磺胺吡啶(SASP)和2 g/L N-乙酰半胱氨酸(NAC)的饲料喂养,模型组及阴性对照组给予普通饲料喂养.评价大鼠肠黏膜病理组织学评分.应用电泳迁移率改变分析法检测肠黏膜胞核NF-κB活性的变化.应用Western印迹分析法检测肠黏膜细胞质IκB及COX-2的变化.应用半定量RT-PCR检测COX-2 mRNA的表达.结果: 姜黄素改善IBD模型大鼠病理组织学征象.姜黄素可抑制IBD模型大鼠肠黏膜胞质IκB的降解,并抑制胞核NF-κB的激活,同时降低了COX-2的活性.结论: 姜黄素可预防和改善IBD鼠科模型中的实验性肠炎,调控COX-2的活性;COX-2可作为治疗炎症性肠病的药物靶点.姜黄素对治疗IBD有应用前景.     

5-氨基水杨酸灌肠对大鼠免疫性结肠炎的影响

目的 探讨5-氨基水杨酸(5-ASA)灌肠对大鼠三硝基苯磺酸(TNBS)诱导的结肠炎的作用.方法用TNBS诱发大鼠结肠炎.造模7天后,用不同剂量的5-ASA(25、50、100mg·kg-1·d-1)开始灌肠.观察大鼠粪隐血(OB)反应强度、结肠大体形态和组织学改变,并检测肠黏膜髓过氧化物酶(MPO)活性.结果 5-ASA灌肠可明显降低结肠黏膜损伤指数(CMDI)、OB反应强度、MPO活性及组织学评分(HS),各剂量组间有一定的量效关系.结论 5-ASA灌肠对TNBS诱导的大鼠结肠炎有保护作用,且与剂量有一定关系.     

4-氨基水杨酸对三硝基苯磺酸诱导的大鼠结肠炎模型的影响

目的:观察4-氨基水杨酸(4-ASA)治疗三硝基苯磺酸(TNBS)诱导结肠炎的疗效并探讨其作用机制. 方法:直肠给予雌性SD大鼠TNBS诱导结肠炎,应用4-ASA-Na(100, 200 mg/kg)对其进行治疗,并以5-氨基水杨酸(5-ASA)作为阳性对照,分别于1 wk及2 wk后取结肠标本评价炎症程度及指标检测,结肠炎症的评价包括大体形态损伤、组织学变化和髓过氧化物酶(MPO)活性,生化法检测超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平,逆转录-多聚酶链反应(RT-PCR)检测结肠组织白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-αmRNA表达水平. 结果:与模型组比较,4-ASA低剂量组和高剂量组的大体和组织学评分均降低(P均＜0.05),MPO活性降低(P＜0.05),SOD活性升高(P＜0.05),MDA水平降低(P＜0.05),IL-1β和TNF-α水平降低(P均＜0.05). 与5-ASA组相比,其疗效无显著性差异. 结论:4-ASA对TNBS诱导的大鼠结肠炎具有良好的疗效,其具有抗氧化作用,可减少IL-1β和TNF-α的生成,从而减轻症状和结肠炎性损伤.     

双歧杆菌对实验性大鼠结肠炎中热休克蛋白70的影响

目的 观察实验性结肠炎热休克蛋白(HSP70) 、白介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)表达变化并研究双歧杆菌对其表达的影响.方法 40只SD大鼠随机均分为正常组、模型组、5-ASA组及双歧杆菌组.2,4,6-三硝基苯磺酸(TNBS)/乙醇制备大鼠结肠炎模型.5-ASA组给予奥沙拉秦钠胶囊100 m...     

铁苋菜水提取液对三硝基苯磺酸诱导的大鼠溃疡性结肠炎的防治作用

目的:考察铁苋菜水提取液对溃疡性结肠炎(UC)的防治作用.方法:雄性SD大鼠70只,随机分为7组,每组各10只.利用三硝基苯磺酸(TNBS)乙醇溶液复制大鼠UC模型,以柳氮磺胺吡啶作为治疗对照药,从大鼠体质量变化、腹泻与便血的动物数、结肠组织形态学改变及组织内髓过氧化物酶(MPO)的活性等多方面考察了铁苋菜水提取液高(9.5 g/kg)、中(6.5 g/kg)、低剂量(2.5 g/kg)治疗及中剂量(6.5 g/kg)预防给药对UC的防治作用.结果:铁苋菜水提取液中、高剂量治疗及中剂量预防给药能够显著改善TNBS模型大鼠体质量的减轻,减少发生腹泻和便血的动物(P<0.05);并且能够显著改善大鼠结肠组织损伤及病理学改变.通过测定各组大鼠结肠组织中MPO的活性,发现铁苋菜水提取液中、高剂量治疗及中剂量预防给药能够显著降低模型组大鼠结肠组织中炎性细胞浸润及MPO的水平(P<0.05),并且与治疗药柳氮磺胺吡啶没有显著性差异.结论:铁苋菜对TNBS诱导的大鼠UC有一定防治作用,具有开发利用价值.     

来氟米特对三硝基苯磺酸诱导的大鼠结肠炎模型的影响

目的观察来氟米特(Lef)对三硝基苯磺酸(TNBS)诱导大鼠结肠炎的保护作用,并初步探讨其作用机制。方法以TNBS诱导大鼠结肠炎模型,将大鼠随机分为6组:正常对照组、模型组、阳性药物对照组(5-ASA100mg/kg,ig,qd×14d)及Lef低剂量、中剂量和高剂量组(1.0、2.0、4.0mg/kg,ig,qd×14d)。每天观察疾病活动指数(DAI),2周后处死大鼠,并取出结肠组织进行大体形态及组织学评分。以免疫组化方法检测结肠组织核因子NF-κBp65、TNF-α的表达,Elisa法测外周血IL-10的含量。结果与TNBS模型组相比,Lef组大鼠的DAI、大体形态、组织学评分及肠黏膜组织内NF-κBp65和TNF-α表达显著降低(P<0.01);大鼠结肠黏膜组织NF-κBp65在模型组以胞核表达为主,相反正常对照组及治疗组NF-κBp65以胞质表达为主;外周血中IL-10含量显著增加(均P<0.01)。结论Lef对TNBS诱导的大鼠结肠炎有抑制作用,其机制可能是通过提高抗炎细胞因子的水平,抑制NF-κB核结合活性,进而降低致炎细胞因子的表达完成。     

四神丸改善TNBS及DSS诱导小鼠实验性结肠炎的研究

目的 观察四神丸对三硝基苯磺酸(TNBS)和低分子量硫酸葡聚糖钠(DSS)诱导的小鼠实验性结肠炎的防治作用.方法 小鼠麻醉后直肠内灌注含1.5 mg TNBS的50％乙醇溶液制备TNBS结肠炎模型;小鼠自由饮用含3％ DSS的蒸馏水5d制备DSS结肠炎模型.各模型均在造模第2天开始灌胃给四神丸,连续8d.观察小鼠的一般状态和结肠炎疾病活动度指数(DAI)评分、结肠组织学及结肠中髓过氧物酶(MPO)变化.结果 TNBS及DSS模型小鼠DAI评分及结肠组织中MPO活性显著高于对照组,模型小鼠可见结肠黏膜上皮脱落、大量炎细胞浸润及腺管扭曲等.经四神丸治疗后能显著改善TNBS及DSS结肠炎小鼠的一般状况及DAI评分,并能改善结肠的组织学损伤、减轻炎细胞的浸润.结论 四神丸对TNBS及DSS所诱导的小鼠结肠炎均有显著的改善作用.     

三硝基苯磺酸诱导的慢性胰腺炎模型在疼痛研究中的应用

目的探讨三硝基苯磺酸(trinitrobenze sulfonic acid,TNBS)建立的慢性胰腺炎(chronic pancreatitis,CP)模型在CP腹痛研究中的适用性。方法 2%TNBS逆行胆胰管灌注建立大鼠CP模型。观察血清淀粉酶、脂肪酶和组织学以评价造模是否成功。Von Frey Filament测试检测不同时间点(1、2、3和4周)大鼠腹部的阳性反应,进而推测大鼠胰腺疼痛的改变。结果 TNBS处理4周后,大鼠胰腺出现实质损伤和进行性纤维化,具有CP的组织病理学改变。Von Frey Filament检测显示CP造模后,随着时间推移,大鼠腹部阳性反应逐渐增加。结论 TNBS不但适用于CP动物模型的建立,而且还适用于CP疼痛的基础研究。     

金黄色葡萄球菌核酸酶对2,4,6-三硝基苯磺酸诱导的小鼠结肠炎的保护作用

探究金黄色葡萄球菌核酸酶(SNase)对2,4,6-三硝基苯磺酸(TNBS)诱导小鼠结肠炎的改善作用及机制。用2.5%TNBS溶液灌肠雌性BALB/c小鼠建立结肠炎模型,并连续6 d灌胃给予以重组乳酸菌为递呈载体的SNase。探究SNase介导的中性粒细胞胞外诱捕网(NETs)的降解对小鼠结肠炎的影响。实验分为正常组、TNBS模型组、NZ9000乳酸菌组、表达SNase的重组乳酸菌组。每日观测小鼠体质量、粪便性状和粪便隐血情况,观察期结束取结肠组织进行HE病理分析,检测结肠组织髓过氧化物酶(MPO)酶活和促炎细胞因子的mRNA表达水平,检测血清炎性细胞因子含量,同时免疫组化检测结肠组织中性粒细胞及其NETs标志物的表达水平。结果表明,乳酸菌递呈的SNase能缓解TNBS诱导的结肠炎小鼠体质量下降,降低疾病活动指数(DAI)评分,缓解结肠缩短并减轻病理损伤,降低结肠组织MPO酶活及炎性细胞因子表达,同时改善了血清炎性水平,免疫组化结果表明结肠组织Ly6G和citH3水平下降。初步机制表明,SNase能够下调炎性细胞因子的表达,降低NETs水平从而缓解小鼠结肠炎。     

Efficacy of Topical versus Oral 5-Aminosalicylate for Treatment of 2,4,6-Trinitrobenzene Sulfonic Acid-induced Ulcerative Colitis in Rats简

5-aminosalicylic acid（5-ASA） is drug of choice for the treatment of ulcerative colitis（UC）. In this study, the efficacy of topical versus oral 5-ASA for the treatment of UC was examined as well as the action mechanism of this medication. A flexible tube was inserted into the rat cecum to establish a topical administration model of 2,4,6-trinitrobenzene sulfonic acid（TNBS）-induced UC. A total of 60 rats were divided into sham operation group（receiving an enema of 0.9% saline solution instead of the TNBS solution via the tube）, model group, topical 5-ASA group, oral Etiasa group（a release agent of mesalazine used as positive control） and oral 5-ASA group（n=12 each）. Different treatments were administered 1 day after UC induction. The normal saline（2 mL） was instilled twice a day through the tube in the sham operation group and model group. 5-ASA was given via the tube in the topical 5-ASA group（7.5 g/L, twice per day, 100 mg/kg）, and rats in the oral Etiasa group and oral 5-ASA group intragastrically received Etiasa（7.5 g/L, twice per day, 100 mg/kg） and 5-ASA（7.5 g/L, twice per day, 100 mg/kg）, respectively. The body weight was recorded every day. After 7 days of treatment, blood samples were drawn from the heart to harvest the sera. Colonic tissues were separated and prepared for pathological and related molecular biological examinations. The concentrations of 5-ASA were detected at different time points in the colonic tissues, feces and sera in different groups by using the high pressure liquid chromatography（HPLC）. The results showed that the symptoms of acute UC, including bloody diarrhea and weight loss, were significantly improved in topical 5-ASA-treated rats. The colonic mucosal damage, both macroscopical and histological, was significantly relieved and the myeloperoxidase activity was markedly decreased in rats topically treated with 5-ASA compared with those treated with oral 5-ASA or Etiasa. The mRNA and protein expression of IL-1β, IL-6, and TNF-α was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. The concentrations of 5-ASA in the colonic tissue were significantly higher in the topical 5-ASA group than in the oral 5-ASA and oral Etiasa groups. It was concluded that the topical administration of 5-ASA can effectively increase the concentration of 5-ASA in the colonic tissue, decrease the expression of proinflammatory cytokines, alleviate the colonic pathological damage and improve the symptoms of TNBS-induced acute UC in rats.     

原花青素B2对三硝基苯磺酸结肠炎模型小鼠肠炎及肠屏障的保护作用

目的探讨原花青素B2（PCB2）对三硝基苯磺酸（TNBS）诱导的结肠炎小鼠肠炎及肠屏障的保护性作用及可能机制。方 法选取6~8周龄雄性Balb/c小鼠，建立TNBS结肠炎小鼠模型，将造模成功的小鼠随机分为PCB2治疗组（n=10）和对照组（n= 10）。PCB2治疗组小鼠每日给予PCB2灌胃（100 mg/kg，0.2 mL），对照组每日给予0.2 mL生理盐水灌胃。4周后处死小鼠，采 用H&E、免疫荧光及免疫印迹法等评估疾病症状、肠道炎症、肠粘膜细胞屏障功能和结构及PI3K/AKT信号改变情况。结果 PCB2治疗组小鼠疾病活动指数在干预第3周和第4周均低于对照组小鼠（P<0.05），而平均体质量在干预第3周和第4周均高于 对照组小鼠（P<0.05）。PCB2 治疗组小鼠结肠炎症评分及肠粘膜炎症介质白介素-1β及肿瘤坏死因子-α水平低于对照组（P< 0.05），而白介素-10高于TNBS组（P<0.05）。PCB2治疗组小鼠肠粘膜对硫氰酸荧光素-葡聚糖通透性及肠系膜淋巴结细菌移位阳 性率均低于对照组（P<0.05）。Western blot检测及半定量分析显示PCB2治疗提高了TNBS模型小鼠claudin-1及ZO-1的表达水 平（P<0.05）。同时，PCB2治疗组小鼠肠粘膜p-PI3K及p-AKT表达水平低于对照组，差异具有统计学意义（P>0.05）。结论PCB2 可能通过抑制肠道PI3K/AKT信号途径发挥抗炎及肠粘膜功能和结构保护作用，可能会成为克罗恩病治疗新的药物选择。     

败酱草提取物对三硝基苯磺酸诱导的大鼠结肠炎的保护作用

目的 观察败酱草提取物对实验性结肠炎大鼠的保护作用.方法 健康SD大鼠随机分组,采用三硝基苯磺酸(TNBS) 125 mg/kg建立结肠炎大鼠模型,灌胃用药4周后,检测各组大鼠结肠组织形态学改变及结肠组织内髓MPO、SOD活性及MDA水平,考察败酱草提取物对大鼠溃疡性结肠炎(UC)的影响.结果 败酱草各剂量组大鼠结肠组织学损伤明显改善(P＜0.05),SOD活性显著高于模型组(P＜0.01),MPO活性、MDA水平显著低于模型组(P＜0.01).结论 败酱草提取物对TNBS诱导的大鼠溃疡性结肠炎有一定的治疗作用,抗氧化应激可能是其作用机制之一.     

别旁茶提取物对实验性炎症性肠病大鼠的作用

目的 探讨别旁茶(BPC)提取物对三硝基苯磺酸(TNBS)诱导的大鼠炎症性肠病的保护作用.方法 采用TNBS灌肠建立炎症性肠病动物模型,造模结束后处死动物检测大鼠结肠组织形态学改变,检测血清肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)、白介素6(IL-6)、白介素27(IL-27)、过氧化物酶(MPO)、超氧化物歧化酶(SOD)的水平.结果 TNBS成功诱导急性实验性肠炎大鼠,与对照组相比,别旁茶提取物可显著改善TNF-α、IL-1β、IL-6、IL-27、MPO、SOD的水平(P＜0.05),别旁茶高剂量组大鼠结肠组织学损伤明显改善(P＜0.05).结论 别旁茶提取物对实验性炎症性肠病大鼠具有显著的保护作用.     

大鼠乙酸性结肠炎模型的实验研究

目的建立大鼠乙酸性结肠炎的模型。方法60只Wistar大鼠随机分为正常对照组、模型对照组、用药组各20只,模型对照组和用药组,用乙酸灌肠建立大鼠溃疡性结肠炎模型后,分别给予生理盐水、醋酸泼尼松(5mg／kg)灌胃,各组采用结肠粘膜损伤指数(CMDI)评分,生化法检测组织中MPO,MDA,SOD,GSH—PX值。结果肉眼观察评分和病理切片组织学评分的结果显示：阳性对照组与模型组之间有统计学差异。MPO测定结果显示阳性对照组MPO低于模型组,与正常组比较,MPO活性仍然较高。阳性对照组结肠粘膜SOD、GSH—PX活性高于模型组,但低于正常组,相反,阳性对照组结肠粘膜MDA含量却低于模型对照组,但高于正常组。结论大鼠乙酸性结肠炎模型作为一种经济,重复性好的动物模型是可用于初步筛选治疗结肠炎的药物,自由基参与溃疡性结肠炎的病理过程。     

细胞因子在大鼠溃疡性结肠炎模型中的表达研究

目的：探讨促炎细胞因子IL-6、TNF-α与抑炎细胞因子IL-10在三硝基苯磺酸（TNBS）/乙醇所致的溃疡性结肠炎（ulcerative colitis,UC）大鼠模型结肠组织中的表达,探讨其在该模型中的作用及意义。方法：雌性SD大鼠随机分为正常对照组及模型组,每组7只。正常对照组不造模,模型组用三硝基苯磺酸（TNBS）/乙醇溶液灌肠复制UC模型。观察两组实验大鼠体质量变化、大体及组织病理学改变,采用酶联免疫吸附法检测细胞因子（IL-6、IL-10、TNF-α）的含量。结果：与正常组比较,模型组大鼠结肠大体形态评分、组织学评分明显升高（0.00±0.00与5.43±1.27,1.29±0.49与6.71±0.95,P〈0.01）;与正常组比较,模型组大鼠结肠组织IL-6、TNF-α表达明显升高（102.13±7.12与188.27±11.65,87.39±6.74与121.51±8.56,P〈0.01）;IL-10表达明显下降（202.97±12.26与71.40±8.28,P〈0.01）。结论：促炎细胞因子IL-6、TNF-α与抑炎细胞因子IL-10的失衡在TNBS诱导的大鼠UC发病中起重要作用。     

Efficacy of thalidomide on trinitrobenzene sulfonate-induced colitis in young rats and its mechanism

Background Thalidomide could relieve clinical symptoms and intestinal mucosal lesions effectively in children with refractory inflammatory bowel disease （IBD） from the pre-clinical study.This study aimed to observe the therapeutic effect of thalidomide by the established animal model of IBD model of 2,4,6-trinitrobenzene sulfonic acid （TNBS）-induced colitis in Sprague-Dawley （SD） rats and to investigate the possible mechanism of action.Methods A total of 82 SD rats of about 4-5 weeks were randomly divided into three groups：the control group （25 rats）,TNBS-treated group （29 rats）,and thalidomide treatment group （28 rats）.Daily activities were recorded.At least eight rats from each group were killed on the 4th,7th,and 14th days.Morphological and histological changes in the colon were individually assessed.Serum was collected and the levels of TNF-α and interleukins （IL-1β and IL-10） were assayed by ELISA method.The expression of colonic mucosal nuclear factor （NF）-KB was assayed with the immunohistochemical method.Results （1） In the control group,diarrhea and rectal bleeding recovered rapidly and no death was recorded.In the TNBS-treated group,diarrhea and rectal bleeding persisted for a longer time.The mortality rate was 10.34％ during the observation period.In the thalidomide treatment group,diarrhea and rectal bleeding persisted for a significantly shorter time than the TNBS-treated group （P ＜0.01）.The rats of this group also exhibited faster weight gain on day 7 compared with the TNBS-treated group but still lower than that of the control group.The mortality rate of the thalidomide treatment group was 3.57％.（2） Macroscopic and microscopic scores of the thalidomide-treated group were significantly lower than those of the TNBS model group on the 14th day （P ＜0.01）.These results suggested faster and better colonic recovery in the thalidomide-treated group.（3） NF-KB expression in the colonic mucosa of the control group was lower than in the others,mainl     

Melatonin reduces acute lung injury in endotoxemic rats

Background Treatment with melatonin significantly reduces lung injury induced by bleomycin, paraquat and ischemia reperfusion. In the present study, we investigated the possible protective roles of melatonin in pulmonary inflammation and lung injury during acute endotoxemia. Methods Thirty-two male Sprague-Dawley rats were randomly assigned to four groups： vehicle ＋ saline group, melatonin ＋ saline group, vehicle ＋ lipopolysaccharide group, melatonin ＋ lipopolysaccharide group. The rats were treated with melatonin （10 mg/kg, intraperitoneal injection （i.p.）） or vehicle （1% ethanol saline）, 30 minutes prior to lipopolysaccharide administration （6 mg/kg, intravenous injection）. Four hours after lipopolysaccharide injection, samples of pulmonary tissue were collected. Blood gas analysis was carried out. Optical microscopy was performed to examine pathological changes in lungs and lung injury score was assessed. Wet/dry ratios （W/D）, myeloperoxidase activity, malondialdehyde concentrations and tumor necrosis factor-alpha （TNF-α） and interleukin-10 （IL-10） levels in lungs were measured. The pulmonary expression of nuclear factor-kappa B （NF-κB） p65 was evaluated by Western blotting. Results PaO2 in the vehicle ＋ lipopolysaccharide group decreased compared with that in the vehicle ＋ saline group. This decrease was significantly reduced in the melatonin ＋ lipopolysaccharide group. The lung tissues from the saline ＋ lipopolysaccharide group were significantly damaged, which were less pronounced in the melatonin ＋ lipopolysaccharide group. The W/D ratio increased significantly in the vehicle ＋ lipopolysaccharide group （6.1±0.18） as compared with that in the vehicle ＋ saline group （3.61±0.3） （P 〈0.01）, which was significantly reduced in the melatonin ＋ lipopolysaccharide group （4.8±0.25） （P 〈0.01）. Myeloperoxidase activity and malondialdehyde levels increased significantly in the vehicle ＋ lipopolysaccharide group compared with that in the vehicle ＋ saline group, which was reduced in the melatonin ＋ lipopolysaccharide group. The TNF-a level of pulmonary tissue increased significantly in the vehicle ＋ lipopolysaccharide group （（8.7±0.91） pg/mg protein） compared with that in the vehicle ＋ saline group （（4.3±0.62） pg/mg protein, P 〈0.01）. However, the increase of TNF-a level of pulmonary tissue was significantly reduced in the melatonin ＋ lipopolysaccharide group （（5.9±0.56） pg/mg protein, P 〈0.01）. Pulmonary IL-10 levels were elevated markedly in the vehicle ＋ lipopolysaccharide group in contrast to that in the vehicle ＋ saline group, whereas the elevation was augmented in the melatonin ＋ lipopolysaccharide group. The nuclear localization of p65 increased markedly in the vehicle ＋ lipopolysaccharide group and this enhancement of nuclear p65 expression was much less in the melatonin ＋ lipopolysaccharide group. Conclusion Melatonin reduces acute lung injury in endotoxemic rats by attenuating pulmonary inflammation and inhibiting NF-κB activation.     

酸吸入致肺损伤对大鼠肺骨形态生发蛋白-4基因表达的影响

目的观察酸吸入致急性肺损伤（ALI）对大鼠肺骨形态生发蛋白-4（BMP-4）mRNA表达的影响。方法HCL（pH=1．5）滴入制备大鼠ALI模型,6小时后处死取肺组织标本,采用RT-PCR方法检测BMP-4 mRNA表达水平。结果对照组BMP-4 mRNA表达水平为0．76±0．06;ALI组为0．87±0．14,较对照组显著升高。结论酸吸入致大鼠ALI使肺组织BMP-4 mRNA的表达受诱导而上调,BMP-4 mRNA表达的改变可能与ALI的发生发展有关。     

Total liquid ventilation reduces oleic acid-induced lung injury in piglets

Background Pediatric patients are susceptible to lung injury that does not respond to traditional therapies. Total liquid ventilation has been developed as an alternative ventilatory strategy for severe lung injury. The aim of this study is to investigate the effect of total liquid ventilation on oleic acid （OA）-induced lung injury in piglets. Methods Twelve Chinese immature piglets were induced acute lung injury by OA. Twelve piglets were randomly treated with conventional gas ventilation （control group） or total liquid ventilation （study group） for 240 minutes. Samples for blood gas analysis were collected before, and at 60-minute intervals after OA-induced lung injury. The degree of lung injury was quantified by histologic examination. The inflammatory cells and the levels of IL-1β, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were analyzed. Results Neutrophil and macrophage counts in bronchoalveolar lavage were significantly decreased in the study group （P〈0.05）. The total lung injury score was also reduced in the study group （P〈0.05）. The concentrations of IL-1β, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were significantly reduced in the study group （P〈0.05）. Conclusions Total liquid ventilation reduces biochemical and histoloaic OA-induced luna iniurv in nialets.