Livin、Caspase-3在结肠腺癌及结肠腺瘤组织中的表达及意义

目的探讨Livin、Caspase-3在结肠腺癌和结肠腺瘤组织中的表达及意义。方法应用免疫组织化学染色方法对89例结肠腺癌、50例结肠腺瘤和40例结肠正常黏膜组织(距癌边缘5 cm以外)进行Livin、Caspase-3检测。应用Western印迹检测方法对50例新鲜结肠腺癌、癌旁组织(距癌边缘5 cm以内)、结肠正常黏膜组织(距癌边缘5 cm以外)进行Livin、Caspase-3检测。结果结肠腺癌组织中Livin阳性率明显高于结肠腺瘤和结肠正常黏膜组织(P<0.05);结肠腺癌组织中Caspase-3阳性率明显低于结肠腺瘤和结肠正常黏膜组织(P<0.05);结肠腺瘤和结肠正常黏膜组织Livin、Caspase-3阳性率有显著性差异(P<0.05)。结论 Livin、Caspase-3在结肠腺癌的发生及发展上起一定作用。     

胃癌组织中Livin与Caspase-9的表达及临床意义

目的 研究Livin和Caspase-9在人体胃癌组织中的表达,初步探讨二者与胃癌生物学行为的关系以及二者之间的相关性.方法 采用免疫组织化学SP法检测78例胃癌组织中Livin和Caspase-9的表达,30例胃溃疡患者胃黏膜组织作为对照.结果胃癌组织中Livin的表达率显著高于对照胃黏膜组织,Caspase-9的表达率则低于对照胃黏膜组织,差异均具有统计学意义(p＜0.01).Livin与Caspase-9的表达呈负相关(P＜0.01,r=-0.304),二者的阳性表达率与肿瘤浸润深度、淋巴结转移、临床分期及肿瘤病理分化程度密切相关,与性别、年龄、肿瘤大小无相关性(P＞0.05).结论 Livin和Caspase-9参与胃癌的发生、发展,二者表达呈负相关.Livin和Caspase-9有可能成为胃癌临床诊断、判断疗效及监测预后的可靠指标.     

黄芪皂甙Ⅳ联合BMSCs移植对大鼠脑缺血再灌注海马神经细胞凋亡及Livin、Caspase-9蛋白的影响

目的 探讨黄芪皂甙Ⅳ联合骨髓间充质干细胞(BMSCs)移植对缺血再灌注大鼠海马Livin、Caspase-9蛋白及神经细胞凋亡表达的影响.方法 实验动物随机分为假手术组、模型组、BMSCs组、联合组.采用线栓法建立大鼠大脑中动脉缺血(MCAO)模型,假手术组不予处理.BMSCs组于造模后3 h移植BMSCs.联合组既移植BMSCs,又给予黄芪皂甙Ⅳ治疗.观察缺血72 h后,各组神经功能评分,PKH-26标记的移植BMSCs分布,采用Western blot和免疫组化方法检测大鼠海马Livin、Caspase-9蛋白的表达,TUNEL方法检测细胞凋亡指数.结果 PKH-26标记的BMSCs在海马有表达.各组中联合组神经功能恢复最为明显(P<0.05).与模型组比较,联合组和BMSCs组均可上调Livin蛋白表达(P<0.05),下调Caspase-9蛋白表达(P<0.05),降低神经元细胞凋亡指教(P<0.05),以联合组作用更为显著(P<0.05).结论 黄芪皂甙Ⅳ联合BMsCs移植对脑缺血再灌注神经元细胞凋亡有协同抑制作用,其作用机制可能与黄芪皂甙Ⅳ促进BMSCs上调Livin蛋白表达,下调Caspase-9蛋白表达,抑制细胞凋亡有关.     

重症急性胰腺炎大鼠肺组织中LIF的表达变化及意义

目的:观察重症急性胰腺炎(SAP)大鼠白血病抑制因子(LIF)在肺组织中表达的时相变化, 探讨LIF在SAP病程及肺损伤中的意义．方法:36只♂SD大鼠随机分为正常对照组(N 组,n=6)、假手术组(Sham组,n=6)和重症急性胰腺炎组(SAP组,n=24)．采用胰管逆行灌注50 g/L牛磺胆酸钠的方法复制大鼠SAP模型．用RT-PCR法检测肺组织中LIF mRNA的表达水平,免疫组织化学方法检测NLIF在肺组织中的表达变化．结果:SAP组3 h后肺组织LIF mRNA的表达量明显高于对照组和假手术组(灰度值:1．018± 0．065 vs 1．451±0．067,1．322±0．072,P<0,05), 并且6,12,24 h持续升高(0．853±0．058,0．635 ±0．064,0．582±0．089)(P<0．01)．同样,SAP组 LIF蛋白表达在3和6 h后明显高于对照组和假手术(127．36±2．76,122．53±2．43 vs 159．46 ±2．78,156．35±3．12,P<0．05),并且12,24 h后也维持在很高的水平(109．37±2．87,102．42± 2．27)．结论:LIF作为促炎症因子参与了SAP肺组织的炎症反应．     

实验性重症急性胰腺炎Caspase-1激活的细胞因子的表达

目的　研究实验性重症急性胰腺炎 (SAP) Caspase- 1激活的细胞因子的表达。方法　 SD大鼠 32只 ,随机分 4组 :正常对照组 (HC组 )、SAP6 h组、SAP12 h组、SAP18h组。采用 5 %牛磺胆酸钠逆行注入胰胆管诱发大鼠 SAP模型。通过 HITACHI- 715 0型自动生化分析仪检测大鼠血清淀粉酶 ;采用 EL ISA法测定血清 IL- 1β水平 ;酶化学法测定胰腺 MPO活性 ;半定量 RT- PCR检测胰腺 Caspase-1、IL- 1β及 IL- 18m RNA的表达 ;免疫组织化学方法检测胰腺 IL- 1β蛋白的表达。结果　 SAP各组血清淀粉酶和 IL- 1β水平显著升高 ,并伴有胰腺组织髓过氧化物酶 (MPO)显著增加 ,与 HC组相比 ,其差异均具有显著性意义 (P<0 .0 1)。HC组胰腺组织内可见 Caspase- 1m RNA表达 ,但 IL- 1β及 IL- 18m RNA的表达较弱 ;SAP各组胰腺组织内 Caspase- 1、IL- 1β及 IL- 18m RNA的表达显著上调 (P<0 .0 1)。 SAP各组 IL- 1β蛋白表达显著增强 ,与 HC组比较差异具有显著意义 (P<0 .0 1) ,而且与 SAP严重程度相一致。结论　 Caspase- 1激活的细胞因子 IL- 1β及 IL- 18的过度表达在 SAP发病机制中发挥重要的作用。     

重症急性胰腺炎大鼠一氧化氮的变化

一氧化氮(Nitric oxide,NO)是生物体内重要的信使和效应分子,参与体内众多的生理病理过程。NO与急性胰腺炎关系密切,动物实验证实,大鼠急性胰腺炎组织中血管内皮细胞和平滑肌细胞以及腹腔巨噬细胞诱导型一氧化氮合成酶(iNOS)表达增强,血清NO含量升高,并参与胰腺组织的损害过程。有关重症急性胰腺炎(SAP)发病过程中NO动态变化国内外较少报道。本文动态观察SAP时大鼠NO水平的变化,旨在进一步探讨SAP的发病机理。     

DCRRT治疗重症急性胰腺炎并急性肺损伤的临床观察

目的探讨日间连续性肾替代疗法（DCRRT）治疗重症急性胰腺炎（SAP）并急性肺损伤（ALI）的临床疗效。方法将40例SAP并ALI患者随机分为DCRRT组、对照组各20例,检测两组治疗前后血浆TNF-α、IL-6、IL-8,比较其生命体征、氧合指数、急性生理与慢性健康评估评分（APACHEⅡ评分）、机械通气时间、ICU住院时间及病死率。结果与对照组比较,DCRRT组TNF-α、IL-6、IL-8下降,生命体征好转,氧合指数提高,APACHEⅡ评分下降,机械通气及ICU住院时间缩短,病死率降低（P〈0.01或〈0.05）。结论 DCRRT能促进SAP并ALI患者的肺功能恢复,减少机械通气时间,缩短ICU住院时间,降低病死率。     

Caspase-9和Caspase-3在血管性痴呆大鼠海马CA1区的表达及意义

目的探讨Caspase-9和Caspase-3在血管性痴呆大鼠海马CAl区的表达及意义。方法将100只大鼠按随机数字法分为假手术组及模型组,每组又分为1、2、4、8和12周5个亚组（n=10只）。采用四血管阻断法制备血管性痴呆模型,应用Morris水迷宫试验检测大鼠的学习记忆能力,TUNEL检测细胞凋亡,免疫组化法检测Caspase-3及Caspase-9蛋白的表达。结果（1）与假手术组比较,在相同时间点模型组大鼠海马CAl区凋亡细胞数明显增多,差异有统计学意义（P〈0．05）;（2）与假手术组比较,模型组大鼠海马CAl区Caspase-9、Caspase-3阳性表达在1周开始增多,2周达到高峰,4周开始下降,到12周仍增多,差异有统计学意义（P〈0．05）。结论Caspase-9及Caspase-3共同参与了血管性痴呆大鼠海马CAl凋亡的调控。     

重症急性胰腺炎合并急性多发性轴索及肌损害一例

患者 ,男 ,35岁 ,干部 ,汉族 ,已婚。主诉 :上腹持续剧痛2 d。现病史 :发病前 2 d饮酒 ,次晨起床后突然剧烈上腹痛 ,恶心 ,呕吐胃内容物 ,无发热。疼痛呈持续性 ,在院外给抗感染治疗无缓解。既往有“胃病”史 ,饮酒史。体检 :T36 .8℃ ,P12 5次 / min,R16次 / m in,BP10 0 / 70 mm Hg,急性病容 ,神清 ,检查合作。皮肤、巩膜无黄染 ,腹平软 ,左中上腹压痛明显 ,无反跳痛 ,移动性浊音 (- ) ,肠鸣音无异常 ,生理反射存在 ,病理反射未引出。实验室检查 :WBC16 .8× 10 9/ L,L 8.8% ,N88.8% ,M2 .4 % ,ESR34m m/ h,尿常规 Glu+ + + ,KET+…     

重症急性胰腺炎并发肾损害的发病机制

重症急性胰腺炎(severe acute pancreatitis,SAP)发病凶险,病情发展迅猛,由胰腺的局部炎症很快发展成具有潜在危险的全身炎性反应,死亡率高,死亡原因多为并发其他重要脏器功能衰竭．其最大的特点就是疾病一旦开始,病情常会不断加重,远离胰腺的脏器损伤程度可以超过原发病灶,甚至造成多器官功能衰竭而死．在临床上,其并发的脏器功能障碍主要有休克、呼衰、肾衰等．SAP引起的肾损害不但可加重胰腺炎的病情,也可发展成肾功能衰竭,导致患者死亡．研究发现,大量炎性介质造成的损害、微循环变化及细胞凋亡等因素可能在其发病机制中起着重要作用．     

Caspase-1 inhibition alleviates acute renal injury in rats with severe acute pancreatitis

AIM:To assess the effect of inhibition of caspase-1 on acute renal injury in rats with severe acute pancreatitis(SAP).METHODS:Forty-two Sprague-Dawley rats were randomly divided into three groups:healthy controls(HC,n=6),SAP rats treated with saline(SAP-S,n=18),or SAP rats treated with a caspase-1/interleukin(IL)-1β-converting-enzyme(ICE)inhibitor(SAP-I-ICE,n=18).SAP was induced by retrograde infusion of 5%sodium taurocholate into the bile-pancreatic duct.HC rats were subjected to identical treatment and surgical procedures without sodium taurocholate.Rats received an intraperitoneal injection of isotonic saline(SAP-S)or the inhibitor(SAP-ICE-I)at 2 and 12 h after induction of acute pancreatitis.Surviving rats were sacrificed at different time points after SAP induction;all samples were obtained and stored for subsequent analyses.The levels of blood urea nitrogen(BUN)and creatinine(Cr)were measured using automatic methods,and serum IL-1βconcentrations were measured by an enzymelinked immunosorbent assay.Intrarenal expression of IL-1β,IL-18 and caspase-1 mRNAs was detected by RT-PCR.IL-1βprotein expression and the pathologic changes in kidney tissues were observed by microscopy after immunohistochemical or hematoxylin and eosin staining,respectively.RESULTS:The serum levels of BUN and Cr in the SAP-S group were 12.48±2.30 mmol/L and 82.83±13.89μmol/L at 6 h,23.53±2.58 mmol/L and 123.67±17.67μmol/L at 12 h,and 23.60±3.33 mmol/L and125.33±21.09μmol/L at 18 h,respectively.All were significantly increased compared to HC rats(P<0.01for all).Levels in SAP-ICE-I rats were significantly decreased compared to SAP-S rats both at 12 and 18 h(P<0.01 for all).Serum IL-1βlevels in the SAP-S group were 276.77±44.92 pg/mL at 6 h,308.99±34.95pg/mL at 12 h,and 311.60±46.51 pg/mL at 18 h;all significantly higher than those in the HC and SAP-ICE-I groups(P<0.01 for all).Intrarenal expression of IL-1βmRNA was weak in HC rats,but increased significantly in SAP-S rats(P<0.01).ICE inhibition significantly decreased the expression of IL-1βand IL-18 mRNAs(P<0.05 for all vs SAP-S),whereas caspase-1 mRNA expression was not significantly different.Weak IL-1βimmunostaining was observed in HC animals,and marked staining was found in the SAP-S group mainly in renal tubular epithelial cells.IL-1βimmunostaining was significantly descended in SAP-ICE-I rats compared to SAP-S rats(P<0.05).Caspase-1 inhibition had no effect on the severity of kidney tissue destruction.CONCLUSION:The expression of caspase-1-activated cytokines IL-1βand IL-18 plays a pivotal role in acute renal injury in rats with experimental SAP.Caspase-1inhibition improves renal function effectively.     

生大黄对重症急性胰腺炎并发肾损伤大鼠的治疗作用

[目的]探讨生大黄在大鼠重症急性胰腺炎(SAP)并发肾损伤时的治疗作用。[方法]将30只雄性SD大鼠随机分为假手术组、SAP组和治疗组,每组10只。采取4.5%牛磺胆酸钠胰胆管逆行注射制备大鼠SAP模型,治疗组在复制模型后即刻胃管内注入生大黄粉溶液。光镜下观察胰腺组织和肾组织的病理损害程度,测定肾脏组织湿干重比,检测各组大鼠血肌酐(Cr)和血尿素氮(BUN)含量,应用RT-PCR方法检测肾脏组织中肿瘤坏死因子-α(TNF-α)mRNA表达。[结果]治疗组大鼠肾脏湿干重比、Cr及BUN明显低于SAP组(P<0.01、<0.05、<0.05);假手术组未见TNF-αmRNA表达,与SAP组相比,治疗组TNF-αmRNA表达明显下降(P<0.05)。[结论]生大黄可以减轻胰腺组织和肾脏组织炎症程度,起到缓解病情、改善肾脏功能和促进修复的作用。     

Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats

AIM： To observe the effect of proteasome inhibitor MG-132 on severe acute pancreatitis （SAP） and associated lung injury of rats. METHODS： Male adult SD rats were randomly divided into SAP group, sham-operation group, and MG-132 treatment group. A model of SAP was established by injection of 5% sodium taurocholate into the biliary- pancreatic duct of rats. The MG-132 group was pretreated with 10 mg/kg MG-132 intraperitoneally （ip） 30 min before the induction of pancreatitis. The changes in serum amylase, myeloperoxidase （MPO） activity of pancreatic and pulmonary tissue were measured. The TNF-α level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay （ELISA） kit. Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed. RESULTS： MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-α level, pancreatic and pulmonary MPO activity （P 〈 0.05）. Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity （P 〈 0.05）. CONCLUSION： The proteasome inhibitor MG-132 shows a protective effect on severe acute pancreatitis and associated lung injury of rats.     

Therapeutic effects of caspase-1 inhibitors on acute lung injury in experimental severe acute pancreatitis

AIM： To assess the therapeutic effect of Caspase-1 inhibitors （ICE-I） on acute lung injury （ALI） in experimental severe acute pancreatitis （SAP）.
METHODS： Forty-two SD rats were randomly divided into 3 groups： healthy controls （HC, n = 6）; SAP-S group （n = 18）; SAP-ICE-i group （n = 18）. SAP was induced by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. HC rats underwent the same surgical procedures and duct cannulation without sodium taurocholate infusion, in SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis and a repeated injection after 12 h. In SAP-ICE-I group, the rats were firstly given ICE inhibitors intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, the injection was repeated at 12 h. Serum 1L-1β was measured by EUSA. Intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were detected by semi-quantitative RT-PCR. The wet/dry weight ratios and histopathological changes of the lungs were also evaluated.
RESULTS： Serum IL-1β levels in SAP-S group were 276.77 ± 44.92 pg/mL at 6 h, 308.99 ± 34.95 pg/mL at 12 h, and 311.60 ± 46.51 pg/mL at 18 h, which were increased significantly （P 〈 0.01, vs HC）. in SAP- ICE-I group, those values were decreased significantly （P 〈 0.01, vs SAP-S）. intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were observed in the HC group, while they were increased significantly in the SAP-S group （P 〈 0.01, vs HC）. The expression of IL-lβ and IL-18 mRNA were decreased significantly in the SAP- ICE-I group （P 〈 0.01, vs SAP-S）, whereas Caspase-1 mRNA expression had no significant difference （P 〉 0.05）. The wet/dry weight ratios of the lungs in the SAP-S group were increased significantly （P 〈 0.05 at 6 h, P 〈 0.01 at 12 h and 18 h, vs HC） and they were decreased significantly in the SAP-ICE-I group （P 〈 0.05, vs SAP-S）.Caspase-1 inhibitors ameliorated the severit     

重症急性胰腺炎肺损伤内皮素的变化及丹参的治疗作用

目的:探讨重症急性胰膜炎(SAP)肺损伤时血清和肺组织内皮素(ET)变化及丹参的保护作用．方法:Wistar大鼠60只,随机分为假手术组(J 组)、模型组(F组)和丹参治疗组(D组)．50 g／L 牛磺胆酸钠胰胆管逆行注射方法制作SAP模型．D组大鼠分别在造模前1 d和造模后10 min ip丹参注射液(5 mL／kg)．各组在制模后24 h及 48 h测定血清ET-1水平及其在肺组织(光密度) 表达情况,同时观察肺系数变化及肺组织病理学改变．结果:与J组比较,F组24和48 h肺组织损伤明显加重,血清ET-1水平(F组:75．8±4．8,70．4± 4．8 ng／L;J组:32．0±6．9,30．3±4．8 ng／L)和肺系数显著增高(F组:0．62±0．06,0．73±0．07;J 组:0．41±0．08,0．41±0．07)(P<0．01),肺组织24 和48 h ET-1表达增高(F组:0．48±0．09,0.61± 0．10;J组:0．05±0．01,0．05±0．01)(P<0．01)．与 F组比较,D组24和48 h肺组织学损伤明显减轻,血清ET-1水平和肺系数明显下降(60．2± 7．3 ng／L,0．52±0．06,P<0．05;57．9±5．43 ng／L, 0．58±0．06,P<0．01),肺组织ET-1表达明显减少(0．23±0．10,0．36±0．09,P<0．01)．相关性分析显示,造模后24和48 h肺组织ET-1表达与肺系数密切相关(r=0．736,P<0．01;r=0．828, P<0．01)．结论:ET-1在SAP肺损伤中起着重要的作用, 丹参对SAP肺损伤具有保护作用．     

Protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis

AIM: To investigate the protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis (SAP). METHODS: One hundred and eighty SD rats were randomly assigned to the model group, Baicalin-treated group, octreotide-treated group and sham operation group. The mortality, plasma endotoxin level, contents of blood urea nitrogen (BUN), creatinine (CREA), phospholipase A2 (PLA2), nitrogen monoxide (NO), tumor necrosis factor (TNF)-alpha, IL-6 and endothelin-1 (ET-1) in serum, expression levels of renal Bax and Bcl-2 protein, apoptotic indexes and pathological changes of kidney were observed at 3, 6 and 12 h after operation. RESULTS: The renal pathological changes were milder in treated group than in model group. The survival at 12 h and renal apoptotic indexes at 6 h were significantly (P<0.05) higher in treated group than in model group [66.67% vs 100%; 0.00 (0.02)% and 0.00 (0.04)% vs 0.00 (0.00)%, respectively]. The serum CREA content was markedly lower in octreotide-treated group than in model group at 3 h and 6 h (P<0.01, 29.200+/-5.710 micromol/L vs 38.400+/-11.344 micromol/L; P<0.05, 33.533+/-10.106 micromol/L vs 45.154+/-17.435 micromol/L, respectively). The expression level of renal Bax protein was not significantly different between model group and treated groups at all time points. The expression level of renal Bcl-2 protein was lower in Baicalin-treated group than in model group at 6 h [P<0.001, 0.00 (0.00) grade score vs 3.00 (3.00) grade score]. The Bcl-2 expression level was lower in octreotide-treated group than in model group at 6 h and 12 h [P<0.05, 0.00 (0.00) grade score vs 3.00 (3.00) grade score; 0.00 (0.00) grade score vs 0.00 (1.25) grade score, respectively]. The serum NO contents were lower in treated groups than in model group at 3 h and 12 h [P<0.05, 57.50 (22.50) and 52.50 (15.00) micromol/L vs 65.00 (7.50) micromol/L; P<0.01, 57.50 (27.50) and 45.00 (12.50) micromol/L vs 74.10 (26.15) micromol/L, respectively]. The plasma endotoxin content and serum BUN content (at 6 h and 12 h) were lower in treated groups than in model group. The contents of IL-6, ET-1, TNF-alpha (at 6 h) and PLA2 (at 6 h and 12 h) were lower in treated groups than in model group [P<0.001, 3.031 (0.870) and 2.646 (1.373) pg/mL vs 5.437 (1.025) pg/mL; 2.882 (1.392) and 3.076 (1.205) pg/mL vs 6.817 (0.810) pg/mL; 2.832 (0.597) and 2.462 (1.353) pg/mL vs 5.356 (0.747) pg/mL; 16.226 (3.174) and 14.855 (5.747) pg/mL vs 25.625 (7.973) pg/mL; 18.625 (5.780) and 15.185 (1.761) pg/mL vs 24.725 (3.759) pg/mL; 65.10 (27.51) and 47.60 (16.50) pg/mL vs 92.15 (23.12) pg/mL; 67.91+/-20.61 and 66.86+/-22.10 U/mL, 63.13+/-26.31 and 53.63+/-12.28 U/mL vs 101.46+/-14.67 and 105.33+/-18.10 U/mL, respectively]. CONCLUSION: Both Baicalin and octreotide can protect the kidney of rats with severe acute pancreatitis. The therapeutic mechanisms of Baicalin and octreotide might be related to their inhibition of inflammatory mediators and induction of apoptosis. Baicalin might be a promising therapeutic tool for severe acute pancreatitis.     

趋化因子CXCL11及其受体CXCR3在重症急性胰腺炎相关肺损害中的作用

目的:制作大鼠重症急性胰腺炎(severe acute pancreatitis,SAP)模型,检测不同时间点趋化因子CXCL11及其受体CXCR3在SAP肺组织中的动态变化,探讨他们在SAP肺功能损害过程中的作用.方法:48只SD大鼠,雌雄不限,随机分为2组:对照组(C组),SAP组(P组),每组24只.4%牛黄胆酸钠逆行胰胆管注射建立SAP大鼠模型,剂量为1mL/kg,C组打开腹腔后仅仅翻动胰腺组织数次.每组随机分为4个亚组,每个亚组6只.4个组分别在1、3、6、12h抽血、处死,留取组织标本.分别检测各不同时间点组的血清淀粉酶、肺湿干重比,胰腺组织、肺组织病理,免疫组织化学法检测肺CXCL11及CXCR3的表达,酶联免疫吸附试验(ELISA)检测血清中的CXCL11的水平.结果:P组各亚组血清淀粉酶值明显升高(P<0.01vsC组);肺湿干重比值:P组3、6、12h组较C组明显升高(P<0.05);胰腺组织、肺组织病理:3、6、12hP组肺组织损伤明显;免疫组织化学显示P组CXCL11与CXCR3蛋白表达较C组表达明显增强(P<0.05),ELISA显示:1、3、6、12hP组血清CXCL11蛋白较C组明显增高(P<0.01).结论:CXCL11/CXCR3可能参与大鼠SAP急性肺功能损害的发病过程.