IL-38对胶原诱导性关节炎大鼠Th17/Treg失衡的调节作用

目的探讨IL-38对胶原诱导性关节炎Th17/Treg失衡的调节作用。方法 SPF级SD大鼠30只,随机分为3组,即正常对照组(CON)、胶原诱导性关节炎大鼠(collagen-induced arthritis rats,CIA)、CIA+IL-38(5ng/g)组;CIA组、IL-38组采用大鼠尾根部皮下注射牛II型胶原乳剂建立CIA大鼠模型;IL-38组于初次免疫后第24天起每天注射IL-38(20-152)5 ng/g,连续给药10d;观察大鼠后足及关节情况,HE染色观察大鼠滑膜组织病理变化,流式检测Th17/Treg细胞变化,ELISA、qRT-PCR检测Th17/Treg相关基因的表达情况。结果 IL-38明显改善胶原诱导性关节炎大鼠的症状、滑膜组织病理情况、调节Th17/Treg细胞的表达水平以及Th17/Treg相关基因的表达水平。结论 IL-38通过调节Th17/Treg失衡对胶原诱导性关节炎大鼠具有保护作用。     

核因子-κB诱骗剂局部应用对胶原诱导性关节炎大鼠治疗作用的研究

探讨核因子-κB诱骗剂(NF-κB decoy)局部应用对Ⅱ型胶原诱导关节炎(CIA)大鼠的治疗作用及其对滑膜基质金属蛋白酶-3(MMP-3)、IL-17、TGF-β表达的影响。建立Ⅱ型胶原诱导大鼠关节炎模型,用NF-κB诱骗剂注射到大鼠右后踝关节腔内,并设对照组、CIA模型组和实验组。42d后观察各组关节炎指数、病理指标,采用ELISA法检测各组大鼠关节液中IL-17、IL-12和TGF-β的水平,免疫组织化学方法检测关节组织MMP-3、TGF-β和IL-17表达。与对照组比较,CIA模型组大鼠关节炎指数、关节液中IL-17、IL-12水平均明显升高,滑膜组织MMP-3、IL-17阳性表达的积分光密度(IOD)值明显增加;实验组经NF-κB诱骗剂注射后,与CIA模型组比较,关节炎指数、关节液中IL-17、IL-12水平均明显降低,而TGF-β的含量显著增高,滑膜组织MMP-3、IL-17阳性表达的IOD值明显降低,TGF-β阳性表达的IOD值显著增高。NF-κB诱骗明显减轻CIA大鼠的关节炎症状,延缓关节破坏的进展,对CIA有较好的治疗作用。     

甲氨蝶呤对脂多糖诱导大鼠滑膜细胞株RSC-364分泌IL-17和IL-18的影响

目的:观察甲氨蝶呤对脂多糖诱导大鼠滑膜细胞株RSC-364分泌IL-17和IL-18表达的影响,进一步探讨甲氨蝶呤治疗类风湿性关节炎(RA)的作用机理.方法:运用ELISA检测不同浓度的甲氨蝶呤对脂多糖诱导大鼠滑膜细胞株RSC-364细胞上清液中的IL-17和-IL-18的含量.结果:甲氨蝶呤明显抑制脂多糖诱导大鼠滑膜...     

基于JAK2-STAT3信号通路探讨硫酸羟氯喹治疗佐剂性类风湿性关节炎大鼠的作用机制

目的 观察硫酸羟氯喹对胶原诱导性关节炎大鼠(CIA)的治疗作用及其可能的作用机制.方法 24只SPF级SD大鼠,随机分为对照组、模型组及硫酸羟氯喹组,每组8只.给药前(0 d)和给药10、20及30 d后进行关节炎指数评分;HE染色观察各组大鼠膝关节滑膜病理损伤;ELISA检测大鼠血清中IL-1β、TNF-α及IL-6水平;Western blot检测大鼠滑膜组织中Bcl-2、Bax及Caspase-3蛋白表达;TUNEL染色观察大鼠膝关节滑膜细胞凋亡情况;Western blot检测大鼠滑膜组织中JAK2、p-JAK2、STAT3及p-STAT3蛋白表达.结果 硫酸羟氯喹显著降低大鼠关节炎指数评分(P＜0.05);减轻大鼠膝关节滑膜病理损伤(P＜0.05);降低血清中IL-1β、TNF-α及IL-6水平(P＜0.05);增加大鼠滑膜组织中Bax、Caspase-3蛋白,降低Bcl-2蛋白表达,抑制大鼠滑膜组织细胞凋亡(P＜0.05);此外,硫酸羟氯喹亦降低了大鼠滑膜组织中p-JAK2与p-STAT3蛋白表达(P＜0.05).结论 硫酸羟氯喹对胶原诱导性关节炎大鼠具有一定的治疗效应,其作用机制可能与抑制JAK2-STAT3信号通路相关.     

昆明山海棠对CIA大鼠足爪组织MMP-13蛋白表达及血清和足爪组织中IL-12、IL-23和IL-37水平的影响

目的:探讨昆明山海棠(Tripterygium hypoglaucum Hutch,THH)对胶原性关节炎(collagen-induced arthritis,CIA)大鼠的干预作用及可能的机制。方法:SD大鼠50只,随机分为正常组和胶原性关节炎模型制作组,用鸡Ⅱ型胶原诱导制作CIA大鼠模型。将造模成功的36只大鼠随机分为模型组、地塞米松治疗组与THH 200 mg/kg、400 mg/kg干预组。ELISA法检测CIA大鼠血清和足爪组织中促炎因子IL-12、IL-23和抑炎因子IL-37的含量;HE染色观察各组大鼠足爪组织病理学变化;Western blot法检测足爪组织MMP-13蛋白的表达;荧光标记法检测大鼠足爪组织中MMP-13的活性。结果:较模型组比较,THH 400 mg/kg治疗组大鼠体重下降明显减轻(P0.01),血清中IL-12和IL-23的水平分别降低了28.31%和41.57%(P0.01),足爪组织中IL-12和IL-23的含量分别下降了30.78%和39.46%,而血清和足爪组织中IL-37的水平显著升高了79.43%和75.78%(P0.01),足爪皮下组织病理变化明显减轻,足爪组织中MMP-13蛋白表达降低了49.22%(P0.01),且MMP-13活性明显下降。而THH 200 mg/kg治疗组大鼠上述指标无明显改善。结论:THH对CIA大鼠炎症的明显抑制作用可能与其降低促炎因子IL-12和IL-23、增高抑炎因子IL-37含量,抑制炎性细胞浸润及血管增生、下调MMP-13蛋白表达、降低MMP-13活性有关。     

诱骗受体DcR3对佐剂型关节炎大鼠模型的作用分析

目的 研究诱骗受体DcR3 对佐剂型关节炎(AA)大鼠模型的作用及其机理.方法 注射弗式完全佐剂建立大鼠佐剂型关节炎(AA)模型,尾静脉注射DcR3蛋白,观察大鼠关节肿胀度、间接 ELISA 检测血清和滑膜液中细胞因子IL-1 β、TNF-α、IFN-γ的变化.RT-PCR检测滑膜和淋巴细胞中DcR3、Fas、FasL mRNA的表达以及脾脏中TGF-β、IFN-γ、TNF-α、IL-4、IL-10 mRNA的表达.Western blot分析滑膜细胞中Caspase-8、Caspase-3、Caspase-9、Bcl-2蛋白的表达.结果 DcR3 治疗AA大鼠后,足肿胀度降低;血液和滑膜液的IL-1β、TNF-α、IFN-γ水平下降;脾脏中TGF-β、IFN-γ、TNF-α mRNA 表达下调,IL-4、IL-10 mRNA表达上调;滑膜细胞中Caspase-8、Caspase-3蛋白表达上调,Bcl-2蛋白表达下调. 结论 DcR3 可以用于实验性大鼠AA的治疗,其治疗机制与调节滑膜细胞FasL、Fas mRNA的表达和血液淋巴细胞中 Fas mRNA的表达,促进滑膜细胞和自身反应性淋巴细胞的凋亡;调节脾脏细胞Th1/Th2细胞因子平衡相关.本研究为进一步阐明RA的发病机理奠定了重要基础,为有效治疗RA提供了新思路.     

IL-18在大鼠抗肾小球基底膜肾炎凋亡中作用的研究

目的:探讨IL-18在大鼠抗肾小球基底膜肾炎细胞凋亡中的作用。方法:复制大鼠抗GBM肾炎模型,分别于实验第2、7、14、21和28天,行以下处理:收集24小时尿、血清样本检测大鼠24小时尿蛋白、血肌酐及血尿素氮含量;取肾组织经光镜、电镜观察肾组织病理变化;采用TUNEL法检测大鼠肾组织细胞凋亡情况;RT-PCR、免疫组织化学和Western blot法分别检测肾组织中IL-18、Fas mRNA和蛋白表达情况。结果:与正常对照组相比,肾炎模型组24小时尿蛋白、血肌酐和血尿素氮含量均明显升高(P0.01);光镜和电镜观察到肾小球内可见新月体形成、GBM不规则增厚、足突融合等病变;肾小球内凋亡细胞于第2天开始轻度增加,随后继续增加,于第28天有所减少,但仍维持较高水平;血清IL-18含量第2天开始升高,此后一直维持较高水平;肾组织中IL-18、Fas mRNA和蛋白表达均显著增加(P0.01);且肾炎模型组血清、肾组织IL-18表达与Fas表达均呈正相关(P0.01)。结论:IL-18在大鼠抗GBM肾炎凋亡中发挥重要的促进作用。     

THH对胶原诱导型关节炎小鼠Th17细胞及细胞因子的影响

目的通过观察昆明山海棠(Tripterygium hypoglaucum hutch,THH)对胶原诱导型关节炎(collagen induced arthritis,CIA)小鼠Th17细胞及相关炎性细胞因子的影响,探讨THH治疗类风湿关节炎的相关免疫学机制。方法 30只健康雄性C57BL/6小鼠随机选取10只作为正常对照组,剩余20只用于制备CIA小鼠模型。将造模成功的小鼠随机分为CIA模型组、THH治疗组,每组9只。通过观测小鼠体质量、关节炎指数评分、关节肿胀程度及HE染色了解THH治疗情况,利用流式细胞术、实时荧光定量PCR(RT-qPCR)及ELISA观察THH对CIA小鼠Th17细胞及IL-17A的影响,并使用GraphPad软件对结果进行分析。结果CIA模型组小鼠体质量与THH治疗组间无统计学差异;关节炎指数评分及关节肿胀程度CIA模型组均高于THH治疗组;HE染色显示THH治疗组关节炎的炎症较模型组减轻,骨损伤减少。流式结果显示,脾脏Th17细胞比例CIA模型组低于正常对照组(P0.01),THH治疗组高于CIA模型组(P0.05)。CIA模型组踝关节及血清中IL-17A表达明显高于正常对照组(P0.01),THH治疗组中的表达量低于CIA模型组(P0.05)。结论 THH可通过升高CIA小鼠外周免疫器官Th17细胞比例、降低关节组织及血清IL-17A表达水平,从而减轻关节炎的炎症反应,减少关节骨损伤。     

DcR3 对肝纤维化动物模型的影响

目的:研究DcR3 基因对肝纤维化大鼠的预防性治疗的作用。方法:SPF 级健康雄性Wistar 大鼠30 只,体重范围180 ~220 g,随机分为3 组,每组10 只,分别为正常对照组、DcR3 基因预防性治疗组(1% DMN+DcR3 组)、造模组(1%DMN 组)。采用1%DMN 诱导大鼠肝纤维化模型,腹腔注射DcR3 质粒进行预防性干预。分别采用HE 染色和Masson 染色观察肝组织病理情况;qRT-PCR 和Western blot 法检测DcR3、Fas、FasL、-SMA 和TGF-1 的mRNA 和蛋白表达水平。结果:与模型组相比,DcR3 预防治疗组大鼠肝组织炎性细胞浸润及胶原类物质沉积有所改善;DcR3 基因可显著降低肝纤维化大鼠Fas、FasL、 SMA 和TGF-1 mRNA 和蛋白表达水平,DcR3 基因预防性治疗组与对照组和造模组有显著性差异(P<0.05);同时DcR3 基因预防性治疗组DcR3 mRNA 和蛋白表达水平显著升高(P<0.05)。结论:DcR3 基因可有效防治大鼠肝纤维化,其作用机制可能是DcR3 通过降低肝脏炎症反应,减少胶原类物质沉积,抑制 SMA 和TGF-1 表达,从而抑制HSC 活化;下调Fas和FasL 表达,抑制Fas/ FasL 途径诱导的肝细胞凋亡。     

IL-4/IL-10诱导的树突状细胞对类风湿性关节炎的作用

目的:探讨经IL-4/IL-10诱导的树突状细胞(DC)对类风湿性关节炎的作用。方法:用Percoll分层离心法从脾脏细胞分离得到DC后,用IL-4或IL-10或IL-4+IL-10进行诱导。用未经诱导和诱导过的DC对类风湿性关节炎大鼠模型进行干扰。SD鼠设为CIA模型组,DC对照组与DC试验组。用ELISA法检测细胞因子与抗体水平,用MTT法检测细胞增殖情况,对鼠爪关节行病理学检测。结果:DC对照组的临床症状评分,病理改变评分,细胞增殖能力,血清中抗胶原抗体及细胞因子水平与CIA模型组的差异无统计学意义。试验组中,注射IL-10-DC能改善CIA鼠的滑膜炎症情况;在初次免疫后第5天注射IL-4-DC能减轻CIA鼠的滑膜炎程度;注射IL-4+IL-10-DC无明显的保护作用。结论:适时注射IL-4或IL-10诱导的DC,对实验性类风湿性关节炎具有保护作用。     

Expression of Fas ligand improves the effect of IL-4 in collagen-induced arthritis

The present study was aimed at investigating whether the expression of Fas ligand (FasL) by CHO cells transfected with IL-4 (CHO/IL-4) or IL-10 (CHO/IL-10) genes would improve the effect of the cytokine. DBA/ 1 mice immunized with type II collagen were treated with suboptimal doses of transfected CHO cells (a single s. c. injection of 2 x 10(5) cells) around onset of arthritis. Severe collagen-induced arthritis (CIA) developed in the control groups injected with PBS, CHO /beta-galactosidase/FasL, CHO/IL-4 or CHO/IL-10 cells. In contrast, administration of CHO/IL-4/FasL, but not CHO/IL-10/FasL, cells significantly reduced the clinical severity and resulted in rapid and sustained suppressive effect. Amelioration of CIA was not due to a prolonged in vivo secretion of IL-4 since expression of FasL by CHO cells shortened the in vivo survival of the xenogeneic cells. In fact, administration of FasL(+) cells was associated with a decreased proportion of Mac1(+) neutrophils in the blood and an increased expression of myeloperoxidase at the site of engineered cell engraftment. These findings suggest that the mechanism underlying the beneficial effect of IL-4 delivered by cells expressing FasL involves the combination of the anti-inflammatory properties of IL-4 and the apoptosis of Fas(+) Mac1(+) granulocytes participating in the pathogenic process.     

Increased synovial expression of IL-27 by IL-17 in rheumatoid arthritis

Objectives and design

Interleukin (IL) 17 plays an important role in synovial inflammation and bone destruction in rheumatoid arthritis (RA), while IL-27 exerts a regulatory role in T cell-mediated immune responses. Our aim was to study the influence of IL-17 on IL-27 production in RA.

Materials and methods

Following injection of IL-17 in the knee joint of CIA mice, synovium was examined for IL-17 and IL-27 expression by western blot, real-time PCR, and immunohistochemistry. IL-17 and IL-27 levels were measured by ELISA in mouse bone marrow-derived dendritic cells (BM-DCs) and in synovial fluid (SF) macrophages from RA patients.

Results

IL-17 exacerbated disease progression in CIA mice. Histological analysis showed increased pannus formation associated with cartilage and bone erosion following injection with IL-17. The expression of IL-27 was increased in CIA mice. The expression of IL-17 and IL-27 was increased more in IL-17-injected CIA mice than in control mice. The majority of cells expressing IL-27 were co-localized with synovial macrophages. Increased expression of IL-27 by application of recombinant IL-17 was confirmed in CIA BM-DCs and in SF macrophages from RA patients.

Conclusion

IL-17 enhanced expression of IL-27 in synovial macrophages from RA patients and CIA mice, indicating an interaction between IL-17 and IL-27 as an autoregulatory mechanism.     

IL-17 increases cadherin-11 expression in a model of autoimmune experimental arthritis and in rheumatoid arthritis

IL-17 plays important roles in synovial inflammation and bone destruction in the mouse model of autoimmune arthritis and in rheumatoid arthritis (RA). Cadherin-11 determines the behavior of synovial cells in their proinflammatory and destructive tissue response in inflammatory arthritis, and promotes the invasive behavior of fibroblast-like synoviocytes (FLS). The purpose of this study was to examine the effect of IL-17 on the expression of cadherin-11 in autoimmune experimental arthritis and in RA synovium. The severity of synovial inflammation and bone destruction were examined in IL-17-injected knee joints of mice with collagen-induced arthritis (CIA). Cadherin-11 expression was examined in the synovium of mice with CIA, of IL-1 receptor antagonist (IL-1Ra)-deficient mice and of patients with RA and osteoarthritis (OA). Cadherin-11 expression was also examined in the synovium of IL-17 injected knee joints from CIA mice and in IL-17-stimulated FLS of CIA mice and RA patients. IL-17 aggravated synovial inflammation and bone destruction in CIA. By immunohistochemistry, cadherin-11 expression was increased in the synovium of mice with CIA and IL-1Ra-deficient mice and in patients with RA. Synovial cadherin-11 expression in IL-17-injected knee joints, measured by real-time RT-PCR, Western blot and immunohistochemistry, was increased in CIA. Cadherin-11 expression was significantly increased by IL-17 in cultured FLS of CIA mice and RA patients, and these increases were blocked by NF-κB inhibitors. IL-17 increased the expression of cadherin-11 in vivo and in vitro, which implies that an IL-17-induced increase of cadherin-11 is involved in IL-17-induced aggravation of joint destruction and inflammation.     

Increased serum IL-10 in lupus patients promotes apoptosis of T cell subsets via the caspase 8 pathway initiated by Fas signaling

We sought to investigate the expression of Fas and FasL on T cell surface and caspase 8 involvement in T cell apoptosis promoted by serum IL-10 in systemic lupus erythematosus(SLE) patients.Cells and sera were obtained from 35 SLE patients.Apoptosis of T cells in patients with SLE was increased and associated with the SLE disease activity index(SLEDAI).Elevated expression of Fas and FasL on T cell surface contributed to increased apoptosis of T cells.Increased IL-10 in the sera of SLE patients was capable of inducing Fas and FasL expression on CD4~+T cell surface,promoting apoptosis of this cell subset.Decreased IL-10 serum levels and low expression of Fas were found in 5 patients of the first follow-up group after 2-month treatment.In another group with one-year treatment,the SLEDAI declined to inactive scores.Serum IL-10 was decreased significantly,and expression of Fas and FasL on T cells was also reduced.Declined apoptosis was predominant only in CD4~+T cell subset.When sera with high level of IL-10 were used to culture PBMCs from healthy controls,activated caspase 8 was elevated in CD3~+T,CD4~+T and CD8~+T cells.The study showed that serum IL-10 induced apoptosis of T cell subsets via the caspase8 pathway initiated by Fas signaling.Increased apoptosis of T cells contributes to autoantigen burden,which is pathogenic in the development of SLE.     

雷公藤多甙对胶原诱导性关节炎大鼠IL-10表达的影响

目的研究雷公藤多甙对类风湿关节炎大鼠的作用,探讨类风湿关节炎的发病机制及雷公藤多甙的作用机制,为临床应用提供理论基础。方法本实验应用鸡Ⅱ型胶原蛋白,建立胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠模型。应用酶联免疫吸附试验方法(ELISA)检测观察正常对照组、CIA模型组和雷公藤多甙治疗组大鼠血液及关节液中白细胞介素-10(interleukin-10,IL-10)的浓度。结果 ELISA检测结果显示,类风湿关节炎大鼠血清和关节液中IL-10含量明显减低,而雷公藤多甙可以升高IL-10的浓度,使之趋向正常。结论雷公藤多甙可有效减轻佐剂型关节炎大鼠的关节病变,并能使CIA大鼠血清、关节浸液IL-10分子水平增高。     

非T 细胞结合肽( FNS007) 对胶原诱导型大鼠关节炎的影响

目的：探讨非T细胞结合肽（FNS007）对大鼠Ⅱ型胶原（Collagen typeⅡ,CⅡ）诱导的关节炎（Collagen-induced arthritis,CIA）的影响及可能机制。方法：以牛CⅡ免疫Lewis大鼠诱发CIA模型后,随机分为模型组、FNS007低（0.25 mg/kg）、中（0.5 mg/kg）、高（1.0 mg/kg）剂量组及阳性药(甲氨蝶呤)组,另设空白对照组,尾静脉注射相应药物,隔天一次,空白对照组及模型组大鼠给予溶媒磷酸盐缓冲液(Phosphate buffered solution,PBS)。实验期间观察踝关节宽度以及爪厚度,关节炎评分。给药后第22天处死大鼠,ELISA法测定血清中TNF-α、IFN-γ和IL-6的水平及抗CⅡ抗体水平;X光分析FNS007对CIA大鼠后爪骨损伤的疗效,并对大鼠踝关节进行组织病理学检查。 结果：FNS007 高剂量明显抑制CIA大鼠足爪肿胀程度,爪厚度和踝关节宽度明显降低;炎症评分明显降低; 血清促炎性细胞因子TNF-α、IFN-γ、IL-6的含量和抗CⅡ抗体的水平明显降低; X光评分和组织病理评分明显降低。FNS007 中剂量和低剂量组的以上指标也有不同程度的改善。 结论：FNS007对大鼠CIA具有治疗作用,其机制与其抑制T细胞活化,抑制CIA大鼠体内抗CⅡ 的产生,并降低促炎性细胞因子TNF-α、IFN-γ、IL-6的含量,从而抑制异常免疫反应有关。     

Caspase-1-independent, Fas/Fas ligand-mediated IL-18 secretion from macrophages causes acute liver injury in mice.

IL-18, produced as a biologically inactive precursor, is processed by caspase-1 in LPS-activated macrophages. Here, we investigated caspase-1-independent processing of IL-18 in Fas ligand (FasL)-stimulated macrophages and its involvement in liver injury. Administration of Propionibacterium acnes (P. acnes) upregulated functional Fas expression on macrophages in an IFNgamma-dependent manner, and these macrophages became competent to secrete mature IL-18 upon stimulation with FasL. This was also the case for caspase-1-deficient mice. Administration of recombinant soluble FasL (rFasL) after P. acnes priming induced comparable elevation of serum IL-18 in parallel with elevated serum liver enzyme levels. However, liver injury was not induced in IL-18-deficient mice after rFasL administration. These results indicate a caspase-1-independent pathway of IL-18 secretion from FasL-stimulated macrophages and its critical involvement in FasL-induced liver injury.     

龟龄集对 AD 小鼠皮层和海马 Fas/ FasL 表达及神经元凋亡的影响

目的 探究龟龄集对阿尔茨海默病 (Alzheimer’s disease, AD) 小鼠皮层和海马 Fas/ FasL 表达及 神经元凋亡的影响。 方法 构建 AD 小鼠模型, 小鼠随机分为对照组、 模型组、 多奈哌齐组及龟龄集低、 中、 高剂量组。 Morris 水迷宫检测干预前后小鼠的学习记忆能力; HE 染色检测小鼠皮层、 海马神经元病理 学改变情况; TUNEL 染色检测神经元凋亡情况; Western 印迹及 Real time PCR 分别检测 Fas、 FasL 的蛋白 表达水平及 mRNA 表达水平。 结果 与模型组比较, 龟龄集各组和多奈哌齐组小鼠学习记忆能力明显提高 (P< 0. 05), 皮层和海马神经元病理学损害及神经元凋亡改善 (P< 0. 05), Fas、 FasL 蛋白和 mRNA 水平下 降 (P< 0. 05)。 结论 龟龄集可能通过抑制 Fas/ FasL 表达抑制 AD 模型小鼠皮层、 海马神经元凋亡, 并改 善其学习记忆能力。     

三七总皂甙对肺缺血再灌注损伤时细胞凋亡及Fas/FasL的影响

目的：探讨细胞凋亡与肺缺血再灌注损伤的关系以及三七总皂甙的作用及机制。 方法: 健康日本大耳白兔84只，随机分为对照组、肺缺血再灌注1、3、5 h组和三七总皂甙干预1、3和5 h组。复制肺缺血再灌注损伤模型。采用原位缺口末端标记（TUNEL）法观测肺组织细胞凋亡指数，免疫组化和原位杂交技术检测肺组织细胞Fas/FasL系统蛋白和基因表达的变化。 结果: 肺缺血再灌注组肺组织细胞凋亡指数和Fas/FasL蛋白及基因表达均显著高于对照组（均P<0.01）。三七总皂甙干预组Fas/FasL mRNA及其蛋白质的表达显著低于缺血再灌注组（P<0.01），肺组织细胞凋亡指数也显著低于缺血再灌注组（P<0.01）。肺组织细胞凋亡指数分别与Fas/FasL蛋白和Fas/FasL mRNA之间均呈显著正相关（r分别=0.540,0.658,0.668,0.686;均P<0.01）。 结论: Fas/FasL系统活化启动的肺组织细胞凋亡可能参与了肺缺血再灌注损伤的发生。三七总皂甙可能通过抑制Fas/FasL系统的激活，阻遏肺组织细胞凋亡，从而减轻肺缺血再灌注损伤。