IL-18激活NF-κB细胞信号通路对人脐静脉内皮细胞损伤作用的体外研究

目的 探讨促炎因子白细胞介素-18(IL-18)通过激活核因子-κB(NF-κB)介导的细胞信号通路 ,对静脉内皮细胞功能的影响及其与深静脉血栓形成(DVT)的联系.方法 利用重组人IL-18作用体外培养的人 脐静脉内皮细胞(HUVECs),并以NF-κB激活抑制剂进行干预,通过实时荧光定量PCR、Western blot、免疫荧 光、流式细胞仪等检测手段,验证IL-18是否通过激活NF-κB介导的细胞信号转导通路,影响HUVECs正常状态及 血管性血友病因子(vWF)、P-选择素(P-selectin)、组织型纤溶酶原激活物(t-PA)等内皮细胞功能标记物 的表达,结合既往研究对IL-18参与DVT的机制进行综合分析.结果 IL-18可激活内皮细胞内NF-κB,使细胞核 内p65表达增高、细胞内IκBα表达降低,并使HUVECs早期凋亡细胞明显增多;添加QNZ(EVP4593)可使IL-18对 NF-κB的激活作用明显抑制,细胞损伤、凋亡的发生显著减少;IL-18可促使vWF、P-selectin和t-PA等DVT相 关的内皮细胞标志物发生表达异常(P<0.05),而各标志物可在NF-κB激活抑制后恢复常规表达.结论 IL-18 及NF-κB间的相互作用导致HUVECs生长状态和功能异常,可能是与DVT发病相关的疾病机制.     

人白细胞介素24基因的克隆及在大肠杆菌中的高效表达

目的：构建人白细胞介素24（hIL-24）基因原核表达载体,在大肠杆菌中诱导表达hIL-24蛋白,并测定其生物学活性。方法：用PCR方法从含有hIL-24的质粒中扩增hIL-24 cDNA序列,测序鉴定正确后,应用基因重组技术构建PQE/hIL-24,并转入大肠杆菌(E.coli)M15。IPTG诱导表达目的蛋白,镍凝胶亲和层析纯化目的蛋白,SDS-PAGE电泳和免疫印迹分析鉴定结果,应用外周血单核细胞（PBMCs）,通过ELESA法分别在48和72 h检测rhIL-24刺激的PBMCs中 IL-6、IFN-γ及TNF-α产生情况。结果：获得与GenBank中报道一致的hIL-24基因片段。SDS-PAGE电泳和免疫印迹分析显示,获得具有hIL-24免疫原性、相对分子质量约为18 400目的蛋白。Ni²⁺-NTA agarose纯化得到单一条带蛋白, 获得rhIL-24蛋白刺激的PBMCs,PBMCs分泌IL-6、IFN-γ、TNF-α的水平显著高于未刺激前分泌水平(P<0.05),rhIL-24具有与天然hIL-24蛋白相同的生物学活性。结论 成功地构建了hIL-24的原核表达载体,在E.coli中高效表达了rhIL-24蛋白,获得了与天然hIL-24蛋白具有相同生物学活性的rhIL-24。     

Modulation of Interleukin-15-induced Suppression of Human Neutrophil Apoptosis by TNFα

Human interleukin-15(IL-15) is a proinflammatory cytokine to suppress neutrophil apoptosis,which is a potential therapeutic agent.The modulatory effect of TNFα was investigated in IL-15-induced suppression of human neutrophil apoptosis.TNFα was shown to reverse the ability of IL-15 to delay neutrophil apoptosis within certain time course.Moreover,this reverse effect by TNFα might be associated with a reduction of the expression of the anti-apoptotic Bcl-Xl protein detected by Western blotting.It is concluded that TNFα can be used to modulate IL-15-induced suppression of neutrophil apoptosis within certain time course.     

Effect of Xuezhikang Capsule(血脂康胶囊)on Serum Tumor Necrosis Factor-αand Interleukin-6 in Patients with Nonalcoholic Fatty Liver Disease and Hyperlipidemia

<正>Objective:To evaluate the effect of Xuezhikang Capsule(血脂康胶囊) on the serum levels of inflammatory factors such as tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in patients with nonalcoholic fatty liver disease(NAFLD) and hyperlipidemia,and to explore whether it has anti-inflammatory effect.Methods:A total of 84 patients were randomly assigned to two groups with stratified block randomization, the treatment group(42 cases) and the control group(42 cases).They were treated with Xuezhikang Capsule and polyene phosphatidylcholine capsule for twenty-four weeks,respectively.The changes in serum TNF-αand IL-6 were measured by enzyme linked immunosorbent assay before treatment and at the 12th and 24th week. Results:Compared with those before treatment,the serum levels of TNF-αand IL-6 significantly decreased in both groups after treatment(P0.01).There was no significant change between the two groups for the treatments at different time points(P0.05) and between the two groups for treatments at the same time points (P0.05).Conclusion:Xuezhikang Capsule can inhibit the serum inflammatory factor in patients with NAFLD and hyperlipidemia.     

人白细胞介素-15cDNA真核表达载体的构建及其在肺癌细胞中的表达

目的观察人ＩＬ－１５ｃＤＮＡ在腺癌细胞内的表达。方法将人ＩＬ－１５ｃＤＮＡ于ＥｃｏＲＩ、ＢａｍＨＩ位点正向克隆到逆转录病毒载体ｐＬＸＳＮ,构建ｐＬ－ＩＬ－１５－ＳＮ的重组质粒。以Ｌｉｐｏｆｅｃｔｉｎ介导将该重组质粒转染到人肺鳞癌细胞（ＰＧ细胞系）和小鼠肺腺癌细胞（ＬＡ７９５细胞系）。经Ｇ４１８条件培养筛选,获得阳性细胞克隆。再经ＣＴＬＬ－２细胞增殖法测阳性细胞ＩＬ－１５的表达活性。结果获得３个ＰＧ细胞和４个ＬＡ７９５细胞阳性克隆,ＩＬ－１５活性测定显示其表达水平在２４ｈ内分别在１４２～２０１或１３８～１７８Ｕ／（ｍｌ·１０６细胞）。结论ＩＬ－１５ｃＤＮＡ转导的人和小鼠肺癌细胞可表达有生物学活性的ＩＬ－１５。     

同型半胱氨酸诱导内皮细胞表达白细胞介素8

目的　探讨同型半胱氨酸是否能诱导培养的人脐静脉内皮细胞表达白细胞介素 8(IL 8)。方法　将培养的人脐静脉内皮细胞经相同浓度同型半胱氨酸处理后 ,采用原位杂交和流式细胞术分别检测其IL 8mRNA和蛋白的表达。结果　原位杂交显示 ,人脐静脉内皮细胞暴露于 0 .1mmol·L-1同型半胱氨酸分别孵育 4h和 8h后 ,其IL 8mRNA表达的平均吸光度值分别为 0 .0 313± 0 .0 0 5 5和 0 .0 4 2 5± 0 .0 0 6 9,均显著高于对照组 (0 .0 197± 0 .0 2 5 1,P <0 .0 1)。方差分析表明 ,各组之间均有显著性差异 (F=16 .5 5 ,P <0 .0 5 )。流式细胞术显示 ,上述实验组的IL 8荧光标记抗体阳性细胞的百分率分别为 34.7%和 38.7% ,均显著高于对照组 (2 9.5 % ,P <0 .0 1)。结论　同型半胱氨酸能诱导内皮细胞表达IL 8,与同型半胱氨酸致动脉粥样硬化作用机制有关     

孕激素对高迁移率族蛋白B1 诱导人脐静脉内皮细胞释放白细胞介素-6 作用的影响

目的 观察孕激素对高迁移率组蛋白B1(HMGB1)诱导人脐静脉内皮细胞(HUNVEC)释放细胞因子白细胞介素-6(IL-6)的影响.方法 分离培养人原代HUVEC,克隆构建HMGB1原核重组表达载体pET14b-HMGB1;用不同浓度的原核表达纯化的HMGB1(0、10、100、500、1000 ng/ml)蛋白和不同浓度的孕酮(0、0.1、1、10、100mmol/L)刺激HUVEC,24 h后用酶联免疫吸附法(ELISA)检测细胞上清中IL-6的表达水平;用500 ng/ml的HMGB1分别与不同浓度的孕酮联合作用刺激培养的HUVEC,ELISA法检测细胞上清中IL-6的表达水平;分析孕酮对HMGB1诱导IL-6影响的剂量效应.结果 不同浓度的HMGB1刺激HUVEC后发现,低浓度HMGB1可轻度下调IL-6的分泌表达,但无明显统计学差异(P>0.05),一定浓度以上则可使IL-6水平明显升高(P<0.01);不同浓度孕激素对HUVEC产生IL-6没有明显影响,但以剂量依赖方式抑制HMGB1对IL-6的分泌(P<0.01).结论 HMGB1可诱导HUVEC释放炎性细胞因子IL-6,而孕激素以剂量依赖的方式抑制这些炎症因子的释放,这为孕激素在内毒素血症的发生发展中发挥保护作用提供了分子水平的理论基础.     

大鼠肝癌模型脾内转染IL-2和(或)IL-12基因对NK细胞的激活作用

目的 :研究脾内直接注射携带 IL- 2和 (或 ) IL- 1 2基因的逆转录病毒包装细胞株对血 IL- 2和 IL- 1 2以及 NK细胞活性的影响。方法 :构建携带 h IL- 2和 (或 ) m IL- 1 2基因的逆转录病毒载体。将肝癌细胞 CBRH3注入大鼠腹腔 ,形成肿瘤 ,断颈处死 ,剖腹取出肿瘤组织 ,剪碎后接种于 5 0只 Wistar大鼠肝脏一叶 ,制备肝癌模型。模型大鼠随机分为生理盐水对照组、空载体对照组、IL- 1 2基因治疗组、IL- 2基因治疗组及 IL- 2 / IL- 1 2联合基因治疗组 ,每组 1 0只。含 IL- 2和 (或 ) IL- 1 2基因的包装细胞于肝癌接种后 1、3、5、7d进行脾内注射转染脾细胞。 EL ISA法检测大鼠血 IL- 2和 IL- 1 2浓度 ,放射性活度测定法检测 NK细胞活性 ,并进行病理学和免疫组化检查。结果 :IL基因治疗后 3d,IL - 2 / IL - 1 2联合基因组血清 h IL - 2与单基因治疗组相比无显著差异。病理示治疗后肝癌组织中淋巴细胞浸润明显增多。 IL治疗组 NK细胞活性较对照组显著增高 (P<0 .0 1 )。治疗后 3d血清 IL达高峰 ,以后逐步下降。 IL - 2 / IL - 1 2联合基因组较 IL单基因组增高 (P<0 .0 5 )。 结论 :脾内直接注射携带 IL -2和 (或 ) IL - 1 2基因的逆转录包装细胞株可明显增强 NK细胞活性 ,IL联合基因治疗优于 IL单基因     

胰蛋白酶对内皮细胞释放IL-10、IL-12和INF-γ的影响

目的研究胰蛋白酶对人脐静脉内皮细胞（HUVECs）释放IL-10、IL-12和INF-γ释放的影响。方法分离、培养HUVECs,倒置显微镜观察原代细胞形态变化,免疫荧光染色检测蛋白酶激活受体2（PAR2）表达,ELISA法检测HUVECs培养上清中IL-10、IL-12和INF-γ水平。结果贴壁后的原代HUVECs经历呈圆形或类圆形、梭性和多角形的形态变化。HUVECs表达PAR2,荧光分布于细胞周边。胰蛋白酶诱导HUVECs上清中的IL-10和IL-12水平显著升高,INF-γ水平几乎未被检出。蛋白酶激活受体-2抑制剂能够降低胰蛋白酶诱导的IL-10和IL-12水平。结论胰蛋白酶可能通过PAR2激活促进内皮细胞释放IL-10和IL-12。     

NLRP3炎症小体介导血管紧张素Ⅱ诱导的人脐静脉血管内皮细胞炎症因子IL-1β的表达

目的研究血管紧张素Ⅱ（AngⅡ）对人脐静脉血管内皮细胞（HUVECs）NLPR3 炎症小体激活与炎症因子白介素-1β （IL-1β）表达的影响。方法体外培养HUVECs,用AngⅡ的不同浓度和刺激时间刺激HUVECs,找到最适合的AngⅡ刺激浓度 与时间。AngⅡ刺激HUVECs前,预用AngⅡ受体阻断剂氯沙坦阻断AngⅡ作用;NAD（P）H抑制剂DPI或H2O2清除剂CAT降 低胞内活性氧（ROS）含量;用caspase-1抑制剂YVAD阻断caspase-1作用;用NLRP3 siRNA沉默胞内NLRP3表达。运用蛋白 印迹法（western blot）分别检测细胞内NOX4、NLRP3、caspase-1以及IL-1β含量。结果（1）HUVECs在浓度10-9MAngⅡ刺激 12 h后,胞内NOX4、NLRP3、caspase-1以及IL-1β的蛋白表达显著增加;（2）氯沙坦、DPI、CAT、YVAD和NLRP3 siRNA都可减 轻AngⅡ诱导的上述反应。结论AngⅡ通过促进HUVECs活性氧生成,激活NLRP3炎症小体,促进胞内炎症介质IL-1β P17活 性片段生成增加,诱导血管炎症的发生。     

人IL—18结合蛋白cDNA的克隆及其逆转录病毒载体的构建

目的：克隆人白细胞介素－18结合蛋白（hIL-18BP)的cDNA及构建hIL-18BP逆转录病毒载体,以研究IL－18BP与IL－18相互作用的机制及自身免疫性疾病的基因治疗。方法：从中国汉族人胎盘组织中提取总RNA,用RT－PCR方法扩增hIL-18BP cDNA,与载体pcDNA3连接,转化大肠杆菌DH5α,得到的重组质粒经鉴定正确后,再作为模板进行PCR,PCR产物插入逆转录病毒载体pLNCX中。结果RT－PCR扩增出全长585bp hIL-18BP cDNA,2次酶切鉴定证明hIL-18BP已分别与pcDNA3,pLNCX重组,2次测序结果均与国外文献报道的hIL-18BP的序列一致。结论：成功地克隆了中国人IL－18BP cDNA,并构建了重组hIL-18BP 闻转录病毒载体。     

Expression of pigment epithelium-derived factor in bladder tumour is correlated with interleukin-8 yet not with interleukin-1α

Pigment epithelium-derived factor (PEDF) is an antiangiogenic factor which is effective in tumour inhibition in a variety of tumours and has not yet been studied in bladder tumour before. In this study the expression of PEDF, interleukin-1α (IL-1α) and -8 (IL-8) in bladder tumours was investigated. Immunohistochemistry was performed on 64 bladder tumour and 23 normal uroepithelium samples. Expression change of the factors was compared with clinicopathological parameters. Correlations between PEDF, IL-1α and IL-8 were analyzed. None of the factors was in relation to gender, tumour occurrence, and size or onset pattern. PEDF (P=0.014) and IL-1α (P=0.049) expression was down-regulated with grade progression. PEDF expression was lower in normal uroepithelium than in papillary urothelial neoplasm of low malignant potential (PUNLMP) (P=0.000) and carcinoma (P=0.009) whilst IL-1α (P=0.000 and P=0.000 respectively) and IL-8 (P=0.000 and P=0.023 respectively) expression was higher in the same grouping. PEDF expression had a negative correlation with IL-8 in PUNLMP (P=0.049, r=-0.578) as well as in tumour grouping (P=0.033, r=-0.276). Deranged expressional change of PEDF, IL-1α and IL-8 could be in relation to loss of differentiation from normal uroepithelium to papillary lesion and eventually to carcinoma.     

Effects of intrinsic nitric oxide on the expression of interleukin-4 and IFN-γ mRNA in the bronchial and lung tissues of sensitized rats

Summary To investigate the effects of intrinsic nitric oxide (NO) on the expression of interleukin-4 (IL-4) mRNA and interferon-γ (IFN-γ) mRNA in the airway inflammation of asthma, the rat models of asthmatic inflammaiton were established by sensitizing and then challenging the animals with ovalbumin. The 24 animals were randomly divided into control group, sensitized group, sensitized and L-Arg-treated group as well as L-NAME-treated group equally. By using in situ hybridization combined with compute physiological quantitative imaging analysis techniques, the influence of intrinsic NO on the expression of IL-4 mRNA and IFN-γ mRNA in the airway inflammatory cells was observed. In situ hybridization study demonstrated that IL-4 mRNA expression was obviously increased as compared with that in the control group, mainly distributed in the inflammatory cells in the submucous of airways in the sensitized group. The increase of intensity of IL-4 mRNA expression was positively correlated with the numbers of eosinophil (Eos) and lymphocyte (both with P < 0.05) in the sensitized group. There was no statistically difference in IFN-γ expression between the control group and the sensitized group. Imaging analysis showed that L-NAME could inhibit the expression of IL-4 mRNA (P < 0.05) and increase the expression of IFN-γ mRNA (P < 0.05), while L-Arg could increase the expression of IL-4 mRNA in inflammatory cells (P < 0.05). It was indicated that a suitable levels of intrinsic NO can influence the expression of IL-4 mRNA of Th2 lymphocytes and the expression of IFN-γ mRNA of Thl lymphocytes and in turn, promote the development of asthmatic airway inflammation.     

细胞因子通过P-38信号通路对内皮细胞蛋白C受体的调节

目的观察肿瘤坏死因子-（TNF-）、白介素-1（IL-1）、干扰素-（IFN-）及白介素-4（IL-4）培养的人脐静脉内皮细胞（HUVEC）内皮细胞蛋白C受体（EPCR）和磷酸化P38（P-P38）的表达。方法分别采用逆转录聚合酶链反应（RT-PCR）、WESTERNBLOT技术测定正常对照组、TNF-组、IL-1组、IFN-组及IL-4组培养的EPCR mRNA、蛋白及P-P38蛋白的表达。结果TNF-组、IL-1组EPCR mRNA含量均较正常对照组低（P〈0.01）。IL-1组、TNF-组EPCR蛋白含量较正常对照组低（P〈0.01或P〈0.05）。TNF-组、IL-1组磷酸化P38蛋白含量均较正常对照组高（P〈0.01）。结论细胞因子TNF-、IL-1可以从基因、蛋白水平减少HUVEC上EPCR的表达,其调节机制可能是通过P38丝裂原活化蛋白激酶途径实现的。     

SA/hIL-15融合蛋白的制备及生物学活性鉴定

目的 制备链亲和素(SA)/人白细胞介素-15 (hIL-15)融合蛋白SA-hIL15和hIL-15-SA,并鉴定其生物学活性.方法 构建原核表达质粒pET24a-6His-SA-hIL-15和pET32a-hIL-15-SA-6His,转化大肠杆菌BL21(DE3),用镍金属螯合(Ni-NTA)层析柱进行纯化,并对其进行复性.CCK-8检测融合蛋白PHA刺激的人外周血淋巴细胞增殖的活性,流式细胞仪分析融合蛋白对生物素化的B16.F10细胞锚定修饰率.结果 成功构建了两种重组融合蛋白的表达质粒并在大肠杆菌实现了高效表达,目标蛋白的表达约占细菌总蛋白的20%.经纯化、复性的SA/hIL-15融合蛋白具有双重活性,即:能促进PHA激活的人外周血淋巴细胞增殖的hIL-15活性,和SA介导的高效结合至表面已生物素化的B16.F10肿瘤细胞的功能(表面锚定修饰效率大于95%).SA-hIL-15双功能融合蛋白促进PHA激活的人外周血淋巴细胞增殖活性高于hIL-15-SA双功能融合蛋白.结论 SA/hIL-15双功能融合蛋白的制备为hIL-15表面锚定修饰的肿瘤细胞疫苗的研制打下了基础.     

腺病毒介导人白介素-10转基因对大鼠同种异体移植血管IL-2、TNF-α的影响

目的:观察腺病毒介导人白介素-10(hIL-10)转基因对大鼠同种异体移植血管IL-2、TNF-α的影响及其可能的作用机制。方法:以Wistar大鼠为供体,SD为受体,采用颈动脉显微外科原位吻合技术,将经直接浸泡法转染腺病毒介导hIL-10的离体供血管植入受体血管。随机分为3组:I组(空白对照组,n=9),II组(空载体组,n=10),III组(基因转染组,n=10)。移植后5d,观察移植物病理组织学变化及免疫排斥级别;RT-PCR、ELISA、免疫组化染色检测移植血管hIL-10基因产物;免疫组化染色检测IL-2、TNF-α。结果:基因转染组移植血管有效地表达特异性hIL-10基因产物。与对照组比较,急性排斥级别降低(P<0.01);IL-2、TNF-α的表达量明显下降(P<0.01)。结论:腺病毒介导人白介素-10转基因能有效地下调IL-2、TNF-α表达,诱导移植血管局部免疫抑制状态,抑制同种异体移植血管的急性排斥反应。     

重组人白细胞介素10基因的克隆及其在真核细胞中的表达

目的：克隆编码人白细胞介素10（hIL-10）基因的全长cDNA,构建真核表达载体,并在中国仓鼠卵巢（CHO）细胞中进行表达.方法：应用逆转录多聚酶链反应（RT-PCR）技术,从活化的正常人外周血单个核细胞中扩增出hIL-10 cDNA,将测序正确的hIL-10 cDNA克隆至真核表达载体pcDNA3构建重组表达载体.采用磷酸钙法转染CHO细胞,用ELISA法检测hIL-10基因的表达,用单四唑（MTT）检测hIL-10蛋白的活性.结果：RT-PCR产物插入Teasy载体,经序列测定证实hIL-10基因全序列克隆成功.在CHO细胞培养上清中有hIL-10的表达,该产物能抑制淋巴细胞转化.结论：成功构建了真核表达质粒pcDNA3-hIL-10,为进一步研究hIL-10在自身免疫、移植免疫及炎症性疾病中的作用打下了基础.     

基于piggyBac转座子系统构建长期表达人细胞因子的免疫缺陷小鼠模型

目的：探讨表达人白细胞介素6（IL-6）、白细胞介素3（IL-3）、白细胞介素15（IL-15）、干细胞生长因子（SCF）和粒细胞-巨噬细胞集落刺激因子（GM-CSF）基因的piggyBac（PB）转座子系统在免疫缺陷小鼠体内的长效表达情况,为改善人源化小鼠模型中人免疫细胞的重建提供简单长效的新方法。方法：构建含有绿色荧光蛋白（GFP）基因的PB转座子质粒（PB-GFP）,构建含有人IL-6、IL-3、IL-15、SCF和GM-CSF基因的PB转座子质粒（PB-5F）。293T细胞分为阴性对照组（未转染质粒）、阳性对照组（转染pLVTHM质粒）、瞬时转染组（转染PB-GFP质粒）和稳定转染组[共同转染PB-GFP和转座酶质粒（super-PB）]。转染后每3 d,采用流式细胞术检测各组细胞中GFP阳性（GFP⁺）细胞百分率。将NOD.Cg-Prkdc^scid IL2rg^tm1Wjl/SzJ（NCG）小鼠分为瞬时转染组和稳定转染组,瞬时转染组小鼠尾静脉高压注射PB-5F质粒,稳定转染组小鼠尾静脉高压注射PB-5F质粒和super-PB质粒。小鼠尾静脉高压注射后1、3、5和9 d及随后每周1次采血分离血清,ELISA法检测各组NCG小鼠血清中IL-6、IL-3、IL-15、SCF和GM-CSF水平。结果：PB-GFP转染293T细胞30 d后,稳定转染组GFP⁺细胞百分率（4.61%±0.42%）明显高于阳性对照组（0.58%±0.05%）和瞬时转染组（0.86%±0.10%）（P<0.05）。NCG小鼠尾静脉高压注射PB-5F质粒,注射后第30天,稳定转染组小鼠血清中IL-6、IL-15和GM-CSF水平均高于瞬时转染组（P=0.048,P=0.051,P=0.045）;注射后第60天,稳定转染组小鼠血清中仍能检测到IL-6、IL-15和GM-CSF。结论：体外验证了PB转座子系统的长效表达,成功构建了具有人IL-6、IL-3、IL-15、SCF和GM-CSF基因的PB转座子载体的质粒,建立了长效稳定表达人IL-6、IL-15和GM-CSF的免疫缺陷小鼠模型。     

Effect of Wumeiwan on Cytokines TNF-α, IL-6, IL-8, IL-10 and Expression of NF-κBp65 in Rats with Ulcerative Colitis

The effects of Wumeiwan （WMW） on TNF-α, IL-6, IL-8, IL-10 and NF-κBp65 in rats with ulcerative colitis （UC） were investigated, the curative effectiveness of WMW vs salicylazosulfapyridine （SASP） was compared, and the action mechanism was analyzed. Fifty-Six Sprague-Dawley （SD） rats were randomly divided into four groups （n=14 in each group, with equal ratio of male and female）： normal control group, model group, SASP group, and WMW group. Except normal control group, the rat UC models in the remaining three groups were established using the method of 2.4-dinitrochlorobenzene （DNCB） immunization and acetic acid local enema. The rats in model group, SASP group, and WMW group were treated with distilled water, SASP, and WMW respectively. The changes in the symptoms and signs were observed, and levels of IL-6, IL-8, TNF-α, IL-10 and the expression of NF-κBp65 in the colonic tissues were statistically analyzed. The results showed that the levels of IL-6, IL-8, and TNF-α were significantly increased （P〈0.01）, while those of IL-10 significantly reduced （P〈0.01） after establishment of rat UC models as compared with normal control group. The levels of IL-6, IL-8, and TNF-α were obviously lower, but the level of IL-10 was obviously higher in WMW and SASP groups than those in model group （P〈0.05）. The levels of IL-6, IL-8, and TNF-α were lower, while the level oflL-10 was higher in WMW group than in SASP group. NF-κBp65 was expressed negatively or weakly in normal colonic tissues. The positive expression rate of NF-κBp65 in WMW group and SASP group was obviously lower than in model group （P〈0.01）, and there was significant difference between WMW group and SASP group （P〈0.05）. It was concluded that rat UC model was established successfully. WMW could up-regulate the expression of IL-10, down-regulate the expression of TNF-α, IL-6, IL-8, and inhibit the NF-κBp65 activity to adjust immune function, indicating WMW had better curative effects on UC in rats.