整合素α4β7在大鼠溃疡性结肠炎发病中的作用

目的 探讨淋巴细胞归巢受体整合素α4β7在溃疡性结肠炎（UC）大鼠发病中的作用.方法 60只SD大鼠分为对照组（20只,仅用丙酮液灌肠）、模型组（2、4-二硝基氯苯丙酮液灌肠,20只）和干预组（造模后即自大鼠尾静脉注入α4抗体,20只）.观察大鼠结肠黏膜损伤情况;采用ELISA法检测结肠组织IL-2和IL-6水平;采用RT-PCR检测结肠组织中α4和β7的表达;采用流式细胞技术检测大鼠门静脉血中整合素α4阳性淋巴细胞数.结果 模型组和干预组大鼠结肠组织α4mRNA相对表达量分别为0.68±0.24和0.58±0.37,β7 mRNA的相对表达量分别为0.84±0.37和0.65±0.30,均显著高于对照组（0.15±0.13,0.24±0.62,均P＜0.01）.模型组和干预组结肠静脉回流血中α4阳性淋巴细胞的比例分别为（76.7±8.2）%和（68.2±7.6）%,显著高于对照组的（14.7±6.7）%（P＜0.01）.与模型组比较,干预组大鼠结肠组织大体损伤评分、组织学评分、IL-2和IL-6水平均显著降低（均P＜0.05）.结论 淋巴细胞整合素α4β7的高表达与大鼠的结肠黏膜炎性反应形成有关,阻断整合素α4β7可有效减轻结肠黏膜炎性损伤.     

整合素α4β7的表达与溃疡性结肠炎大鼠肠淋巴细胞归巢

目的 探讨淋巴细胞归巢受体整合素α4β7的表达与溃疡性结肠炎(UC)大鼠肠淋巴细胞归巢的关系,分析UC大鼠肠道黏膜免疫功能改变的机制.方法 将40只SD大鼠随机分为UC组和对照组,分别于造模后72 h取标本检测:免疫组织化学法检测肠组织中地址素MAdCAM-1;逆转录-聚合酶链反应(RT-PCR)检测肠组织中α4β7的表达;流式细胞检测大鼠门静脉血中整合素α4阳性淋巴细胞数的变化.结果 UC组大鼠结肠黏膜下MAdCAM-1表达明显增强(0.72±0.33比0.21±0.41,P<0.01),主要表达在黏膜下微血管区;UC组α4、β7 mRNA的表达量与对照组比较明显升高(0.683±0.238;0.842±0.374比0.146±0.132;0.241±0.624,P均<0.01);UC组结肠静脉回流血中α4+淋巴细胞的比例明显高于对照组(76.73±8.24比14.66±6.74,P<0.01).结论 UC大鼠发病时α4β7阳性淋巴细胞的比例升高,参与肠淋巴细胞过渡归巢现象,肠黏膜免疫功能亢进可能是UC发病的重要因素.     

葛仙汤治疗大鼠溃疡性结肠炎

目的:探讨葛仙汤对大鼠溃疡性结肠炎的治疗作用及其机制.方法:将SD大鼠按均衡随机原则分为正常对照组、模型对照组和葛仙汤低、中、高剂量组,采用大肠杆菌加乙酸免疫复合法造成大鼠溃疡性结肠炎模型.连续给药21 d,观察动物的一般情况,进行疾病活动指数(DAI)评估、结肠病理学评分(HS),检测血清中IL-6、IL-10含量.结果:葛仙汤低、中、高剂量3个治疗组DAI和HS均明显低于模型对照组(P<0.05或P<0.01),IL-6含量与模型对照组比较均明显减少(P<0.01);中剂量组IL-6含量明显低于高、低剂量组(P<0.05).3个治疗组IL-10均较模型对照组明显升高(P<0.01);中、低剂量组IL-10明显高于高剂量组(P<0.05).结论:低、中、高剂量葛仙汤均能缓解溃疡性结肠炎大鼠的症状,减轻其结肠病理损伤,促进溃疡面愈合,其中以中剂量效果为更好.     

溃疡性结肠炎大鼠淋巴细胞的过渡归巢与CCR7的表达

目的探讨实验性溃疡性结肠炎（UC）大鼠淋巴细胞过渡归巢现象与淋巴细胞表面CCR7受体表达的关系。方法40只SD大鼠随机分为对照组及模型组，观察结肠黏膜下淋巴细胞过渡归巢现象，逆转录-聚合酶链反应（RT-PCR）半定量法检测结肠组织中CCR7的表达；流式细胞法（FCM）测定结肠回流血液中CCR7＋淋巴细胞的比例。结果模型组大鼠结肠黏膜下存在淋巴细胞过渡归巢，派尔集合淋巴结增生，最大截面积比较，差异有统计学意义[（9．56±0．32）比（1．48±0．58），t=5．12，P〈0．01]，CCR7mRNA的表达量与对照组比较明显升高[（0．772d-0．108）比（0．126±0．029），t=4．37，P〈0．01]、模型组结肠静脉回流血中CCR7＋淋巴细胞的比例明显高于对照组[（76．58±9．73）％比（16．62±7．84），t=3．97，P〈0．01]。结论溃疡性结肠炎大鼠的结肠黏膜下存在淋巴细胞过渡归巢现象，结肠组织中归巢受体CCR7的表达增高，结肠回流血液中CCR7＋的淋巴细胞的比例增高。     

淫羊藿对大鼠溃疡性结肠炎的治疗机制研究

目的:观察淫羊藿对大鼠溃疡性结肠炎的治疗效果以及对结肠组织中相关炎症因子表达的影响。方法:雄性SD大鼠84 只,随机分为空白对照组、模型组、淫羊藿高、中、低剂量组、柳氮磺吡啶(SASP)组及联合治疗组,每组12 只。采用疾病活动指数(DAI)、结肠大体损伤评分、结肠组织病理学评分、结肠组织TNF-α、IFN-γ 和IL-6 免疫组化表达情况评价其治疗作用。结果:在实验处理第4 天开始,各实验组大鼠与模型组比较体重增加,实验第7 天联合组大鼠与SASP组比较体重增加,且差异均有统计学意义(P <0.05);第5 天开始各实验组与模型组比较,DAI 评分升高,差异有统计学意义(P <0.05);各实验组结肠损伤程度与模型组比较,联合组的结肠溃疡面积及结肠重量与长度比减小,淫羊藿高、中、低剂量组及联合组的结肠损伤程度减轻,联合组的结肠溃疡面积小于SASP 组,差异均有统计学意义(P <0.05);与模型组比较,淫羊藿高剂量组结肠组织病理学评分显著降低(P <0.01);各实验组大鼠结肠组织中TNF-α、IFN-γ 和IL-6 表达水平,联合组及SASP 组与模型组比较显著降低(P <0.01),联合组较SASP 组显著降低(P <0.01)。结论:淫羊藿可改善溃疡性结肠炎大鼠的精神状态、减轻结肠损伤程度,其治疗作用可能与其减少TNF-α、IFN-γ 和IL-6 细胞因子表达有关。     

RNAi对大鼠T淋巴细胞CD28和OX40基因表达的联合抑制作用

目的 通过RNAi技术干扰T细胞CD28、CD134基因表达后,诱导获得抑制性T细胞(Ts);探讨Ts免疫学特性.方法 设计针对目标基因的siRNA,转染大鼠T淋巴细胞,FCM检测CD28、CD134水平,混合淋巴细胞反应(MLR)检测转染后的T淋巴细胞对异体淋巴细胞的增殖能力的影响,逆转录-聚合酶链反应(RT-PCR)及酶联免疫吸附试验(ELISA)法检测细胞因子水平.结果 siRNA转染大鼠T淋巴细胞后,抑制CD28、CD134分子的表达,siRNA转染24 h后,siRNA组CD28、CD134表达受到抑制[转染后及转染前表达分别为(22.35±4.37)%及(34.76±3.51)%(P<0.05)],T淋巴细胞分泌细胞因子IL-10水平增高,转染组及未转染组表达分别为(77.15±12.60)ng/L及(37.56±5.93)ng/L(P<0.01).而转染组及未转染组的IL-2表达分别为(2.79±0.51)及(4.35±1.11)ng/L(P<0.05);干扰素(IFN)-γ表达分别为(277.15±14.8)、(682.7±53.5)ng/L(P<0.05).结论 siRNA可以特异性抑制大鼠T淋巴细胞共刺激分子CD28、CD134基因表达,抑制了IL-2、IFN-γ的表达,提高了IL-10细胞因子表达水平,从而产生了免疫耐受效应.Ts细胞具有抗原特异性,而且在外源性rrIL-2存在时,不能逆转Ts细胞的功能.     

健脾止泻宁颗粒联合美沙拉嗪治疗溃疡性结肠炎中细胞因子与髓过氧化物酶的关系

目的观察健脾止泻宁颗粒联合美沙拉嗪对溃疡性结肠炎(UC)模型大鼠细胞因子以及结肠组织中髓过氧化物酶(MPO)水平的影响。方法 75只Wistar雄性大鼠采用随机数字表法随机分为5组:正常对照组、模型对照组、健脾止泻宁组、美沙拉嗪组和联合治疗组, 每组15只。采用大鼠疾病活动指数(DAI)评分评估大鼠肠炎症状严重程度的指标。酶联免疫吸附试验(ELISA)检测各组大鼠血清中细胞因子白细胞介素(IL)-1β、IL-4、IL-6、IL-8、IL-10、肿瘤坏死因子-α(TNF-α)、IL-18水平, 蛋白质印迹法(Western blot)检测结肠黏膜组织中MPO的表达。采用单因素方差分析进行统计学分析。结果与正常对照组比较, 模型组及各个给药治疗组DAI评分均增高, 差异有统计学意义(F=128.574, P<0.05);与模型组比较, 各治疗组DAI评分均降低, 差异有统计学意义(F=128.574, P<0.05)。与模型组比较, 健脾止泻宁组、美沙拉嗪组及联合用药组血清IL-1β、IL-6、IL-8、TNF-α和IL-18水平升高(F=90.948、92.243、132.4...     

巨噬细胞移动抑制因子与单核细胞趋化蛋白-1在溃疡性结肠炎发病中的作用

目的:探讨巨噬细胞移动抑制因子(MIF)、单棱细胞趋化蛋白-1(MCP-1)在溃疡性结肠炎发病中的意义.方法:采用ELISA法检潮36倒活动期溃疡性结肠炎(UC)、30例健康体检者血清中MIF、MCP-1含量.结果:UC患者的血清MIF水平(11.402±1.936μg/L)高于正常对照者的血清MIF水平(5.135士1.692μg/L),P<0.05;溃疡性结肠炎重度组的MIF水平高于轻度组(13.647±2.574)μg/Lvs(8.865±1.527)μg/L,P<0.05.活动期uc患者血清MCP -1水平为(227.6±19.4)pg/ml高于对照组(109.2±14.9)pg/ml,P<0.01,溃疡性结肠炎MCP-1量度组的水平高于轻度组(258.1±18,3)pg/mlvs(175.8±16.7)pg/ml,P<0.05.结论:巨噬细胞移动抑制因子(MIF)和单核细胞趋化蛋白-1(MCP-1)参与溃疡性结肠炎的发病过程,可能是溃病性结肠炎活动的指标.     

结肠透析联合药物保留灌肠在溃疡性结肠炎中应用的临床观察

目的 探讨结肠透析联合药物保留灌肠治疗溃疡性结肠炎的效果.方法 对80例溃疡性结肠炎患者按住院时间的顺序分为对照组(38例)和观察组(42例),对照组采取传统清洁灌肠加药物保留灌肠,观察组用结肠透析仪行结肠灌洗,再注入药物保留灌肠治疗.结果 观察组治疗总有效率显著高于对照组(P<0.01);肠道内药物保留时间显著优于对照组(P<0.05).结论 结肠透析联合药物保留灌肠可提高溃疡性结肠炎治疗的效果.     

IL-17A及Th17在炎症性肠病中的作用

目的:检测IL-17A、IL-10、IFN-阍诨航馄谘字⑿猿觃(inflammatory bowl disease,IBD)患者中的表达,探讨诸炎症因子及Th17在炎症性肠病的发病及治疗中的作用.方法:应用ELISA检测12例Crohn病(Crohn disease,CD)、46例溃疡性结肠炎患者(ulcerative colitis,uc)和20例健康人(正常对照组)血清中IL-17A、IL-10和IFN-愕乃剑⒂妹庖咦橹炸检测CD、UC及正常对照组结肠黏膜局部IL-17A的表达.结果:正常对照组结肠黏膜局部未检测到IL-17A的表达,而UC和CD组在结肠黏膜活组织中均检测到IL-17A的表达.同样UC和CD组血清中IL-17A明显增高,而正常对照组血清未检出IL-17A;UC和CD组患者血清IL-10水平均较对照组升高(P<0.05),且CD组明显高于UC组(P<0.05);CD、UC组与正常对照组血清中IFN-愕谋泶锊钜煳尥臣蒲徕襙(P>0.05).结论:IL-17A不仅在缓解期IBD患者结肠黏膜局部表达,同时在其血清中高表达,提示Th17及其分泌的IL-17A在缓解期IBD患者的发病过程中起重要作用,并伴随促炎因子和抑炎性因子失调.     

Claudin-1和Claudin-2在大鼠急性结肠炎黏膜中的表达

目的 观察紧密连接蛋白Claudin-1和Claudin-2在急性结肠炎大鼠模型结肠黏膜中的表达.方法 对16只SD大鼠采用三硝基苯磺酸灌肠建立急性结肠炎模型,各取8只分别于1周和2周后观察结肠组织的病理学变化,另取5只正常大鼠作对照.应用量子点免疫标记技术检测两种蛋白在正常大鼠、结肠炎1、2周大鼠结肠黏膜中的表达及分布,测定蛋白表达的荧光强度.结果 与正常组比较,急性结肠炎1周时大鼠的Claudin-1和Claudin-2表达均明显增强(荧光强度分别为66.01±25.14比48.12±13.25,70.35±24.36比40.12±9.56,P均<0.01)且分布更广,2周时表达水平较1周时回落(P<0.05),其中Claudin-1下降较为明显,Claudin-2仍维持一个较高水平[分别为54.64±14.26和60.87±14.27,与正常组比较,差异均有统计学意义(P<0.05,P<0.01)].Claudin-1和Claudin-2表达的变化与结肠炎病理学观察的结果 基本一致.结论 急性结肠炎导致肠黏膜的Claudin-1和Claudin-2表达增强,尤以Claudin-2增加明显,两者的变化与急性结肠炎的病理改变密切相关.

Abstract：

Objective To study the expression of Claudin-1 and Claudin-2 in colonic epithelium of trinitrobenzene sulfonic acid (TNBS)-induced acute colitis models in rats.Methods Sixteen TNBS-induced colitis models in rats were established, and pathologic changes of colonic epithelium were analyzed after one or two weeks respectively. Fluorescence of quantum dots-labelled Claudin-1 and Claudin-2 expression was detected in colonic epithelial cells of normal, one-week colitis, and two-week colitis rats. Fluorescence intensity and distribubition of fluorescence signals were recorded and analyzed.Results As compared with that in normal rats (n=5), both Claudin-1 and Claudin-2 expression was increased in one-week colitis rats (relative fluorescence intensity: 66.01±25.14 vs. 48.12±13.25, 70.35±24.36 vs 40.12±9.56, both P<0.01) with wider distribution in crypt. In two-week colitis rats, Claudin-1 and Claudin-2 expression levels were dropped, but Claudin-2 expression was decreased less than Claudin-1, and both remained at a higher level than normal rats (54.64±14.26 and 60.87±14.27, respectively, P<0.05 and P<0.01, respectively vs normal). The changes of expression of Claudin-1 and Claudin-2 were in accordance with the results of pathologic scoring for colitis.Conclusion Along with the pathologic changes in colonic epithelium, Claudin-1 and Claudin-2 expression levels are increased in acute colitis rats, and Claudin-2 expression seems more significant than Claudin-1 as an indicator for colitis.     

Pretreating mesenchymal stem cells with IL-6 regulates the inflammatory response of DSS-induced ulcerative colitis in rats

The immunomodulatory properties of mesenchymal stem cells (MSCs) have been broadly investigated in research on inflammatory diseases including ulcerative colitis. Treating MSCs with an inflammatory stimulus before transplantation is an adaptive strategy that helps MSCs survive in areas of inflammation and promotes the regulation of local immune responses. This study aimed to examine the effects of pretreating bone marrow MSCs (BMSCs) with Interleukin-6 (IL-6) on attenuation of dextran sulfate sodium (DSS)-induced ulcerative colitis in rats. Experimental ulcerative colitis was induced in Wistar rats by administering 2% DSS in their water for 7 days and normal water for the next 3 days. The experimental group received 1 × 10⁶/0.4 ml of BMSCs that were treated with IL-6 for 24 h. Histological changes, colon length, and disease activity index were compared among groups, and the levels of TNF-α, IL-6, and IL-1β in homogenate supernatants were evaluated using ELISA. IL-6-pretreated BMSCs significantly reduced the colonic damage score. The colon length shortened by 6.1 ± 0.14 cm for the rats that received IL-6-pretreated BMSCs, whereas the control group rats' value was 3.8 ± 0.14 cm on the 14th day. The levels of pro-inflammatory cytokines were significantly decreased in the colons of the IL-6-pretreated BMSCs group compared with those of the control group (p < 0.05). This study revealed that IL-6-pretreated BMSCs ameliorated DSS-induced colitis via local anti-inflammatory action and suggested that IL-6-pretreated BMSCs are a promising therapeutic agent for ulcerative colitis treatment.     

Vitamin E has a dual effect of anti-inflammatory and antioxidant activities in acetic acid�Cinduced ulcerative colitis in rats

Background

Increased free radical production, decreased antioxidant capacity and excessive inflammation are well-known features in the pathogenesis of inflammatory bowel disease. Vitamin E is a powerful antioxidant and a scavenger of hydroxyl radicals, and it has been shown to have anti-inflammatory activities in tissues. We investigated the effects of vitamin E on inflammatory activities using an acetic acid (AA)–induced ulcerative colitis model in rats.

Methods

Wistar rats were divided into 4 groups. Acetic acid was given to 2 groups of animals to induce colitis while the other 2 groups received saline intrarectally. One AA-induced colitis group and 1 control group received vitamin E (30 U/kg/d) intraperitoneally and the pair groups received saline. After 4 days, we evaluated colonic changes biochemically by measuring proinflammatory cytokine levels in tissue homogenates and by histopathologic examination.

Results

Acetic acid caused colonic mucosal injury, whereas vitamin E administration suppressed these changes in the AA-induced colitis group (p < 0.001). Administration of AA resulted in increased levels of tumour necrosis factor-α, interleukin-1β, interleukin-6, myeloperoxidase and malondialdehyde, and decreased levels of glutathione and superoxide dismutase; vitamin E reversed these effects (all p < 0.001).

Conclusion

Our study proposes that vitamin E is an effective anti-inflammatory and antioxidant and may be a promising therapeutic option for ulcerative colitis.     

Patterns of inflammation in mucosal biopsies of ulcerative colitis: perceived differences in pediatric populations are limited to children younger than 10 years

The histologic criteria used to diagnose ulcerative colitis in colonic mucosal biopsies have been established for many years and include crypt architectural distortion, plasmacellular infiltrates, and neutrophils in the crypt epithelium and lumen. In several recent studies, it has been noted that colonic mucosal biopsies from children presenting with ulcerative colitis show fewer histologic abnormalities at initial presentation, especially less architectural distortion, than do biopsies from adults. In this study, colonic mucosal biopsies taken at the time of presentation of ulcerative colitis in 15 adults and 25 children were examined blindly by two pathologists. All biopsies were taken prior to the initiation of therapy. Twelve children were between 1 and 10 years of age, and 13 children were between the ages of 11 and 17 years. All patients had at least 1 year of follow-up, with clinical and pathologic confirmation of the diagnosis of ulcerative colitis. Five separate histologic features that are characteristic of ulcerative colitis were scored on mucosal biopsies. Children < or = 10 years of age had significantly less crypt branching, plasma cells in the lamina propria, cryptitis, crypt abscesses, and epithelial injury than adults (P values ranging from < 0.0001 to 0.0032). Children between the ages of 11 and 17 years had less cryptitis, crypt abscesses, and epithelial injury than adults (P values ranging from 0.0001 to 0.007) but similar degrees of crypt architectural distortion and plasma cell infiltrates. For all histologic features examined except epithelial injury, the significant findings were due to differences in biopsies taken proximal to the rectum. No significant differences in histology scores were found in rectal biopsies between any age group, except for epithelial injury, which was significantly less in children < or = 10 years. The findings show for the first time that the perceived differences between adults and children with ulcerative colitis are largely due to a decrease in histologic features of colitis in children less than 10 years of age. As children approach adulthood, the degree of inflammation and architectural distortion seen is similar to that found in adults. However, rectal biopsies show similar degrees of colitis in all age groups.     

The In-Vitro Action of Lymphocytes on Autologous Colon Epithelial Cells in Ulcerative Colitis

The action in culture of peripheral blood lymphocytes on autologous large-intestinal epithelial cells was studied in 13 patients with severe mucosal ulcerative colitis. Two different methods were used to measure lymphocyte activity. These showed that autologous-lymphocyte-induced release of isotopic label and detachment in monolayer culture of large-intestinal epithelial cells was increased in acute ulcerative colitis when compared with findings in the same studies in six normal subjects. Subsequently in four of the six patients who responded to cortisone it was shown that lymphocyte activity against epithelial cells returned to the normal range. Further control studies showed little lymphocyte activity against autologous skin and ileum, suggesting that autologous-lymphocyte-induced damage of large-intestinal epithelial cells is a tissue-specific reaction in patients with acute ulcerative colitis. The absence of reactivity in other colonic inflammatory diseases also suggested that such increased in-vitro lymphocyte activity is disease-specific for ulcerative colitis     

不同免疫调节方式对烧伤脓毒症大鼠炎性反应的影响

Objective To investigate the effect of Thymosin and growth hormone(GH) on inflam-matory response in burn rats or burn rats with sepsis. Methods Sixty-four SD rats were randomly divided into normal control group (NC, without treatment), sepsis group (S, with injection of LPS), sepsis + Thy-mosin group (ST, with successive injection of Thymosin and LPS), sepsis + GH group [SGH, with succes-sive injection of recombinant human GH (rhGH) and LPS], burn group, burn + sepsis group (BS, with in-jection of LPS after burn), burn + sepsis + Thymosin group (BST, with successive injection of Thymosin and LPS after burn), burn + sepsis + GH (BSGH, with successive injection of rhGH and LPS after burn), with 8 rats in each group. Specimens of spleen tissues were harvested to determine HLA-DR in lymphocyte and e-valuate inflammatory cell infiltration (score). Specimens of peripheral blood were collected to determine Toll-like receptor 4 (TLR4) level in monocyte and serum level of TNF-α, IL-4, IL-6, IL-10. Results Compared with those in NC group, serum level of IL-10 in S group decreased obviously, while other indices increased obviously (P<0.01). The levels of HLA-DR and TLR4 and serum level of TNF-α were similar between SGH and ST groups (P>0.05). Compared with those in SGH group [(2.87±0.04) score, and IL-6 (0.0083±0.0018) μg/mg, IL-4 (0.0102±0.0021) μg/mg, IL-10 (0.0310±0.0027) μg/mg, re-spectively], degree of inflammatory cell infiltration (1.50±0.76) score and serum levels of IL-6, IL-4, IL-10 of rats in ST group decreased obviously (0.0064±0.0012, 0.0058±0.0024, 0.0230±0.0021 μg/mg, respectively, P<0.01). The levels of HLA-DR, TLR4 and inflammatory cell infiltration degree of spleen in B group were respectively higher than those in NC group and lower than those in BS group. Com-pared with those in NC group, serum levels of TNF-α, IL-6 in B group increased significantly, while IL-4, IL-10 showed an opposite tendency. There was no obvious difference between BST and BSGH groups in ser-um levels of HLA-DR and IL-6 (P>0.05). Compared with those in BST group, inflammatory cell infiltra-tion degree in spleen and the levels of TLR, TNF-α obviously decreased (P<0.01), while IL-4 and IL-10 levels increased in BSGH group (P<0.01). Conclusions Inhibitive effects between Thymosin and GH on extensive inflammatory reaction were similar with or without trauma, and GH has better effect as compared with Thymosin when with trauma.     

二氯甲烷对盲肠结扎穿孔诱导大鼠急性肺损伤的保护作用

目的 观察二氯甲烷对盲肠结扎穿孔模型大鼠急性肺损伤(acute lung injury,ALI)的保护作用.方法 40只SD大鼠按随机数字表法分为SHAM组、CLP组、MC组和DSF+MC组4组,每组10只.10 h后右侧颈总动脉放血处死.左肺行支气管肺泡灌洗,灌洗液进行白细胞计数,检测蛋白浓度和TNF-α及IL-10水平;右肺下叶观察大鼠肺组织病理变化,其他肺叶匀浆后检测丙二醛和髓过氧化物(myeloperoxidasedeficieney,MPO).另取40只大鼠随机分组处理同上,手术后分笼,观察其活动、刺激后反应;记录72 h生存率.结果 CLP组大鼠肺部炎症和损伤明显,与CLP组相比,MC组肺泡壁无增厚,肺泡内炎症细胞浸润减少,肺组织内TNF-α降低(55±16vs 164±36,P<0.01),IL-10增高(534.6±187.6 vs 75.2±26.1,P<0.01),丙二醛降低(7.8±1.7vs 30.4±2.2,P<0.01),术后72 h生存率显著增高(80%vs 0%,P<0.01).与MC组相比,MC+DSF组肺泡壁增厚,肺泡内炎症细胞浸润增多;肺组织内TNF-α增高(138±23 vs 55±16,P<0.01),IL-10降低(138.3±26.4vs 534.6±187.6,P<0.01),丙二醛升高(26.5±1.9 vs 7.8±1.7,P<0.05),术后72 h生存率显著增高(80% vs0%,P<0.01).结论 二氯甲烷对盲肠结扎穿孔所致的ALI具有明显的保护作用.