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| 1 | Effects of probiotic on intestinal mucosa of patients with ulcerative colitis显示文摘AIM: To investigate the effects of probiotic on intestinal mucosae of patients with ulcerative colitis (UC), and to evaluate the role of probiotic in preventing the relapse of UC.METHODS: Thirty patients received treatment with sulphasalazine (SASP) and glucocorticoid and then were randomly administered bifid triple viable capsule (BIFICO)(1.26 g/d), or an identical placebo (starch) for 8 wk. Fecal samples were collected for stool culture 2 wk before and after the randomized treatments. The patients were evaluated clinically, endoscopically and histologically after 2 mo of treatment or in case of relapse of UC. p65 and IκB expressions were determined by Western blot analysis.DNA-binding activity of NF-κB in colonic nuclear extracts was detected by electrophoretic mobility shift assay (EMSA). mRNA expressions of cytokines were identified by semi-quantitative assay, reverse transcriptasepolymerase chain reaction (RT-PCR).RESULTS: Three patients (20%) in the BIFICO group had relapses during 2-mo follow-up period, compared with 14 (93.3%) in placebo group (P<0.01). The concentration of fecal lactobacilli, bifidobacteria was significantly increased in BIFICO-treated group only (P<0.01).The expressions of NF-κB p65 and DNA binding activity of NF-κB were significantly attenuated in the treatment group than that in control (P<0.05). The mRNA expression of anti-inflammatory cytokines was elevated in comparison with the control group.CONCLUSION: The probiotic could impede the activation of NF-κB, decrease the expressions of TNF-α and IL-1β and elevate the expression of IL-10.These results suggest that oral administration of this new probiotic preparation is effective in preventing flare-ups of chronic UC. It may become a prophylactic drug to decrease the relapse of UC. | Hai-HongCui Cun-LongChen Ji-DeWang Yu-JieYang YongCun Jin-BaoWu Yu-HuLiu Han-LeiDan Yan-TingJian Xue-QingChen | 2004 | World Journal of Gastroenterology2004，10，10： | 44 |
| 2 | Expression of NF-кB and human telomerase reverse transcriptase in gastric cancer and precancerous lesions显示文摘AIM:To investigate the expression of NF-κBp65 protein and human telomerase reverse transcriptase (hTERT) and their correlation in gastric cancer and precancerous lesions.METHODS: Forty-one patients with primary gastric cancer,15 with dysplasia, 23 intestinal metaplasia and 10 with normal gastric mucosa were included in this study.Expression of NF-κBp65 protein,hTERT mRNA and protein were determined by immunohistochemistry and in situ hybridization.RESULTS:The rate of p65 expression in normal gastric mucosa, intestinal metaplasia,dysplasia and carcinoma was 0%, 34.78%, 53.33% and 60.98%,respectively,while the rate of hTERT mRNA expression was 10.00%,39.13%,66.67% and 85.37% and the rate of hTERT protein expression was 0%,30.43%,60.00% and 78.05%,respectively.All the three parameters were significantly increased in dysplasia and carcinoma compared to normal mucosa, while the expression levels were also significantly higher in carcinoma than in intestinal metaplasia (P<0.05).In gastric cancer tissues, nuclear staining rates of p65 and hTERT protein were both significantly associated with the degree of differentiation, lymph node metastasis,clinical stage and invasion depth (P<0.05).However,hTERT mRNA expression was only significantly associated with clinical stage.There was a positive correlation between p65 and hTERT mRNA(rs=0.661-0.752, P<0.01),and between hTERT protein and hTERT mRNA (rs=0.609-0.750, P<0.01).CONCLUSION: NF-κBp65 and hTERT expressions are upregulated at the early stage of gastric carcinogenesis.NF-κB activation may contribute to hTERT expression and thereby enhance telomerase activity, which represents an important step in carcinogenesis progress. | WeiWang He-ShengLuo Bao-PingYu | 2004 | World Journal of Gastroenterology2004，10，2： | 30 |
| 3 | 甘草酸二铵对大鼠结肠炎的抗炎作用机制研究显示文摘目的建立大鼠急性期结肠炎模型,观察甘草酸二铵(DG)对大鼠结肠炎的治疗作用,并探讨其抗炎机制。方法雌性SD大鼠分为实验组、模型组和正常对照组,每组10只。实验组、模型组大鼠用冰乙酸灌肠建立急性期结肠炎模型,实验组给予40 mg.kg-1.d-1DG干预治疗。观察疾病活动指数(DAI)、组织学变化及髓过氧化物酶(MPO)活性,免疫组化法检测核因子-κB(NF-κB)、肿瘤坏死因子-α(TNF-α)和细胞间粘附分子-1(ICAM-1)表达。结果实验组、模型组和正常对照组的DAI评分分别为3.5±0.6,7.1±0.8和0.5±0.4;组织学评分为3.5±0.9,6.1±1.0和1.0±0.5;MPO活性为0.72±0.08,2.02±0.10和0.22±0.04;TNF-α阳性率分别为(35.2±8.2)%,(62.5±10.1)%和(7.9±5.7)%;ICAM-1阳性率为(34.3±8.2)%,(60.2±8.3)%和(9.1±3.4)%;NF-κB阳性率为(23.3±9.2)%,(44.5±8.9)%和(9.6±4.4)%。与模型组相比,实验组的DAI、组织学及MPO活性显著改善,实验组的TNF-αI、CAM-1和NF-κB的表达显著降低,经one-way ANOVA及SNK-q检验,差异有统计学意义(P值均<0.01)。结论DG可显著改善大鼠结肠炎症,其机制可能是通过影响炎症反应的信号通路NF-κB活化及ICAM-1、TNF-α的产生和表达来抑制炎症反应。 | 原皓 林三仁 吴克香 顾芳 张红梅 高志星 焦建新 | 2006 | 中华消化杂志2006，26，1： | 24 |
| 4 | 核因子-κB在大鼠实验性溃疡性结肠炎肠组织的表达及其意义显示文摘目的:观察大鼠实验性溃疡性结肠炎肠组织核因子-κB(NF-κB)及TNF-α、ICAM-1的表达,探讨NF-κB在溃疡性结肠炎发病过程中的作用.方法:采用三硝基苯磺酸(TNBS)制备大鼠溃疡性结肠炎模型,设正常组、生理盐水组及轻、重模型组共4组.采用免疫组织化学染色检测肠组织NF-κB、TNF-α和ICAM-1表达,生化方法检测MPO含量,并分析NF-κB活性与肠道病理损伤指数、MPO含量、TNF-α及ICAM-1表达的关系.结果:溃疡性结肠炎大鼠肠组织中NF-κB活性,TNF-α、ICAM-1表达及MPO含量较正常组及生理盐水组显著增高(NF-κB:52.14±9.81、30.26±10.20,60.73±13.41、45.24±10.86vs13.31±4.76、16.95±6.83,11.61±4.85、14.10±5.76;TNF-α:74.50±11.20、48.11±5.95,84.09±14.52、53.40±8.79vs16.99±5.48、20.04±6.76,10.13±1.79、16.03±6.21;ICAM-1:68.15±7.25、44.34±7.54,77.69±8.09、47.01±8.82vs15.34±4.03、17.50±6.95,10.33±2.38、13.41±4.91;MPO:1.69±0.11,0.71±0.06vs0.39±0.07,0.31±0.08;P<0.01),且在病情严重组增高尤为明显.NF-κB表达水平与TNF-α和ICAM-1阳性细胞密度、MPO含量、肠道病理损伤指数呈显著正相关关系(r分别为0.9304,0.8680,0.6865,0.9292,0.8462;P<0.001或P<0.005).结论:NF-κB在溃疡性结肠炎发病过程中可能起重要作用. | 李军华 于皆平 何小飞 徐细明 | 2003 | 世界华人消化杂志2003，11，2： | 24 |
| 5 | CCK-8抑制LPS作用下大鼠肺间质巨噬细胞NF-κB活性的cAMP-PKA通路研究显示文摘目的:用cAMP激动剂forskolin和PKA抑制剂H-89,探讨八肽胆囊收缩素(CCK-8)抑制LPS作用下大鼠肺间质巨噬细胞(PIM s)核因子-κB(NF-κB)活性的cAMP-PKA信号通路机制。方法:分离纯化大鼠PIM s。用电泳迁移率改变分析(EMSA)法检测大鼠PIM s中NF-κB活性,用W estern b lotting分析IκB-α蛋白水平。结果:正常对照组大鼠PIM s核内未检测到与特异性寡核苷酸探针相结合的NF-κB,LPS组细胞内NF-κB活性明显高于正常对照组(P<0.01),胞浆中IκB-α水平显著低于正常对照组(P<0.01)。CCK组和Fsk组细胞内NF-κB活性和胞浆中IκB-α含量均无明显差异(P>0.05)。CCK+LPS组和Fsk+LPS组,细胞内NF-κB活性均低于LPS组(P<0.05),IκB-α含量均高于LPS组(P<0.01)。LPS+CCK+H-89组NF-κB活性高于CCK+LPS组(P<0.01),而IκB-α蛋白水平低于CCK+LPS组(P<0.01)。结论:cAMP-PKA信号通路的活化可抑制LPS诱导的大鼠PIM s细胞内NF-κB活性升高和IκB-α蛋白水平的降低,CCK-8的抗炎作用是通过激活cAMP-PKA信号通路进而抑制NF-κB活性来实现的。 | 高维娟 许顺江 丛斌 李淑瑾 马春玲 徐锦荣 姚玉霞 谷振勇 | 2006 | 中国病理生理杂志2006，22，10： | 20 |
| 6 | 复方苦参注射液对巨噬细胞内NF-kB作用的研究显示文摘目的探讨复方苦参注射液对硫乙醇酸盐(TG)激活的巨噬细胞内NF-kB表达的影响。方法给小鼠腹腔内注射硫乙醇酸盐(TG),3 d后取小鼠腹腔巨噬细胞(m acrophage),进行离体培养,于培养液中加入三个不同剂量组的复方苦参注射液,观察巨噬细胞核内NF-kB(nuclear factor kappa B)的变化。结果复方苦参注射液能显著抑制巨噬细胞内NF-kB的活化,中剂量组与模型对照(con tro l)组间NF-kB p65核移位有显著性差异(P<0.01)。结论实验证实复方苦参注射液其抗炎症作用可能与它抑制巨噬细胞内NF-kB的活化作用有关。以上结果为临床应用复方苦参注射液的抗炎治疗提供了实验依据。 | 孙静文 张伟 | 2005 | 现代检验医学杂志2005，20，5： | 14 |
| 7 | CCK-8对LPS攻击小鼠IL-1β、IL-6、IL-4、IL-10表达的影响显示文摘目的:观察LPS攻击小鼠IL-1β、IL-6、IL-4、IL-10的动态变化规律及八肽胆囊收缩素(CCK-8)对其表达的影响。方法:将小鼠分为4组:对照组、LPS组(腹腔注射LPS)、LPS+CCK-8组(注射LPS前30 min腹腔注射CCK-8)及CCK-8组(单独注射CCK-8)。用ELISA及PT-PCR方法检测各组小鼠血清、肺组织中IL-1β、IL-6、IL-4、IL-10的含量及mRNA的表达情况。结果:LPS攻击可使小鼠血清及肺组织中IL-1β、IL-6、IL-4、IL-10蛋白及mRNA的表达增加,预先注入CCK-8可显著抑制IL-1β、IL-6的表达,并使IL-4、IL-10的表达进一步增加。结论:CCK-8可能通过抑制LPS攻击小鼠IL-1β、IL-6的表达和进一步增加IL-4、IL-10的表达参与抗炎反应过程,从而减轻LPS引起的肺组织炎症反应。 | 倪志宇 丛斌 李淑瑾 马春玲 闫玉仙 徐锦荣 张国忠 | 2007 | 中国病理生理杂志2007，23，2： | 11 |
| 8 | CC-K8抑制LPS诱导的大鼠肺间质巨噬细胞TLR4及IL-1β的表达显示文摘目的观察八肽胆囊收缩素(cholecystokininoctapeptide ,CCK 8)对外源性脂多糖(lipopolysaccharide ,LPS)激活大鼠肺间质巨噬细胞(pulmonaryinterstitialmacrophages,PIMs)Toll样受体4 (Tolllikereceptor4 ,TLR4 )及IL 1β表达的影响,探讨CCK- 8的抗炎作用机制。方法分离培养大鼠PIMs ,经LPS、CCK- 8及溶剂单独或共同孵育不同时间后,采用Northernblot、ELISA、RT PCR技术检测TLR4mRNA、IL- 1β及IL- 1βmRNA表达的变化。结果LPS(1mg/L)刺激可使PIMs中TLR4mRNA表达明显增强;随着LPS孵育时间的延长,细胞中的IL -1β含量逐渐增多,2 4h达高峰,IL- 1βmRNA表达水平同时明显升高;CCK 8可剂量依赖性抑制LPS诱导的大鼠PIMsTLR4mRNA、IL- 1β及IL 1βmRNA的表达。结论CCK 8对LPS激活的PIMsTLR4及IL- 1β表达有负性调节作用,是CCK- 8抗炎作用机制之一。 | 倪志宇 李淑瑾 丛斌 姚玉霞 王春艳 | 2005 | 基础医学与临床2005，25，2： | 10 |
| 9 | Effect of lipopolysaccharide on expression andcharacterization of cholecystokinin receptorsin rat pulmonary interstitial macrophages显示文摘AIM: To investigate the effect of lipopolysaccharide (LPS) on the expression and the binding characteristics of cholecystokinin receptors (CCK-R) in rat pulmonary interstitial macrophages (PIMs). METHODS: The PIMs isolated from rat lung tissues were purified by the collagenase digestion method combined with alveolar lavage and pulmonary vessel perfusion. The expression of CCK-R mRNA was detected by RT-PCR and Southern blot analysis and the binding experiments were performed by radioligand binding assay (RBA). RESULTS: CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were detected in rat PIMs and their RT-PCR amplified products had a size of approximately 1.37 kb and 480 bp, respectively. The relative expression of CCK-BR mRNA was higher than that of CCK-AR mRNA after incubation with LPS for 0.5, 2, and 6 h. The expression of CCK-R mRNA could be upregulated obviously by LPS. Southern blot analysis of RT-PCR amplified CCK-AR and CCK-BR mRNA products using [γ-^32p]ATP 5'-end-labelled probe showed specific hybridization bands. The specific binding of [^3H] CCK-8S to rat PIM membranes was detected in the rats administered with LPS for 48 h, but not in normal rats. Scatchard analysis of the saturation curves suggested the presence of CCK-R with a high affinity (Kd=0.68±0.28 nmol/L) and a low binding capacity (Bmax=32.5±2.7 fmol·mg^-1 protein) in rat PIMs. The specific binding of [^3H] CCK-8S to rat PIM membranes was inhibited by unlabelled CCK-8S (IC50=2.3±0.8 nmol/L), CCK-AR specific antagonist CR1409 (IC50=0.19±0.06 μmol/L) and CCK-BR specific antagonist CR2945 (IC50=3.2±1.1 nmol/L). CONCLUSION: Two types of functional CCK-AR and CCK-BR existed in rat PIMs and their expression could be upregulated by LPS. | Shun-jiangXU Wei-juanGAO BinCONG Yu-xiaYAO Zhen-yongGU | 2004 | Acta Pharmacologica Sinica2004，25，10： | 9 |
| 10 | CCK-8抗炎作用中DAG-PKC信号通路对cAMP-PKA信号通路的影响显示文摘目的探讨CCK-8抗炎作用中DAG-PKC信号通路对cAMP-PKA信号通路的影响。方法分离纯化大鼠PIMs,分别用LPS、CCK、LPS+CCK、PMA、SC-3088、LPS+PMA、LPS+SC-3088、CCK+PMA、CCK+SC-3088、LPS+CCK+PMA、LPS+CCK+SC-3088孵育一定时间,采用125I-cAMP放射免疫分析法测定细胞内cAMP含量,用放射激酶法测定PKA活性。结果单独应用PMA和SC-3088孵育大鼠PIMs,细胞内cAMP含量和PKA活性与正常对照组相比无明显变化(P>0.05)。PMA可升高LPS作用下的细胞内cAMP含量和PKA活性(P<0.01),SC-3088则可使LPS作用下的细胞内cAMP含量和PKA活性降低(P<0.01)。分别应用PMA、SC-3088与CCK共同孵育,则CCK+PMA组细胞内cAMP含量和PKA活性高于单独应用CCK组(P<0.01),CCK+SC-3088组则降低(P<0.01)。与LPS+CCK组相比,PMA+LPS+CCK组细胞内cAMP含量和PKA活性升高(P<0.01),而SC-3088+LPS+CCK组细胞内cAMP含量和PKA活性降低(P<0.01)。结论在LPS诱导的大鼠PIMs,CCK-8可通过激活cAMP-PKA信号通路发挥抗炎作用;DAG-PKC信号通路的活化对cAMP-PKA信号通路有正性调节作用。 | 高维娟 许顺江 丛斌 李淑瑾 马春玲 | 2008 | 中国药理学通报2008，24，9： | 7 |
| 11 | Hepatocellular apoptosis after hepatectomy in obstructive jaundice in rats显示文摘AIM: To investigate the hepatocellular apoptosis after hepatectomy in obstructive jaundice and biliary decompression rats.METHODS: After bile duct ligation for 7 days, rats were randomly divided into OB group in which the rats undervvent 70 % hepatectorny, OB-CD group in which the rats underwent hepatectorny accompanied by choledochoduodenostomy, CDHx group in which the rats underwent choledochoduodenostomy and then received 70 % hepatectomy on the fifth day after biliary decompression. The control group (Hx group) only underwent hepatectorny.RESULTS: The level of total serum bilirubin and serum enzymes was significantly lower in CD-Hx group than in OB-CD and OB groups on day 1, 3 and 5 after hepatectorny. The apeptotic index was significantly lower in CD-Hx group than in OB-CD and OB groups on day 3 and 5. The oligonucleosomal DNA fragments and Caspase-3 activity were also lower in CD-Hx group than in OB-CD and OB groups 3 days after hepatectorny,without differences between CD-Hx and Hx groups.CONCLUSION. Hepatocellular apoptosis plays vital roles in jaundice rats, and biliary decompression is more effective in treatment of patients with severe jaundice before operation. | De-Sheng Wang Ke-Feng Dou Kai-Zong Li Zhi-Qing Gao Zhen-Shun Song Zheng-Cai Liu Department of Hepatobiliary Surgery,Xijing Hospital,the Fourth Military Medical University,Xi’an 710032,Shannxi Province,China | 2003 | World Journal of Gastroenterology2003，9，12： | 7 |
| 12 | 肝硬化性心肌病研究显示文摘肝硬化性心肌病是肝硬化的并发症之一,主要表现为心脏舒张功能减低、心排血量增加、全身血管阻力降低。一旦增加患者的心脏负荷,如对其行肝移植、外科门体分流术、经颈静脉肝内门体分流术等就有可能诱发心力衰竭,因此对其发生、发展以及演变过程的研究显得尤为必要。总结近年来肝硬化性心肌病的研究进展,旨在为临床肝硬化疾病的系统治疗提供帮助。 | 高扬 李国杰 | 2008 | 医学综述2008，14，2： | 6 |
| 13 | Effect of cholecystokinin octapeptide on diacylglyceroI-PKC signaling pathway in rat pulmonary interstitial macrophages stimulated by lipopolysaccharide显示文摘Aim:To investigate the effect of cholecystokinin octapeptide(CCK-8)on thediacylglycerol-protein kinase C(DAG-PKC)signaling pathway in rat pulmonaryinterstitial macrophages(PIM)stimulated by lipopolysaccaride(LPS).Methods:The PIM from rat lung tissues were isolated using the collagenase digestionmethod combined with alveolar lavage and pulmonary vessel perfusion.DAGcontent and PKC activity were measured by radioenzymatic assay.The transloca-tion of PKCζ was determined by semi-quantitative immunoblot analysis.Results:CCK-8,at high concentrations(1×10^(-6)-1×10^(-5)mol/L),decreased DAG content andinhibited PKC activity and PKCζ translocation compared with that in rat restingPIM of a control group(P<0.01).LPS increased DAG content,and promoted PKCactivity and PKC~ translocation(P<0.01).CCK-8 decreased LPS-induced DAGcontent and inhibited LPS-induced PKC activity and PKCζ translocation signifi-cantly at 1×10^(-8)-1×10^(-5)mol/L(P<0.01).This inhibitory effect of CCK-8 could beabrogated partly by proglumide(non-selective CCK receptor antagonist),CR-1409(selective CCK-A receptor antagonist),and CR-2945(selective CCK-Breceptor antagonist)in a concentration-dependent manner(P<0.01).Conclusion:CCK-8 was a negative modulator of the DAG-PKC signaling pathway in rat restingPIM,which is very important for maintaining body homeostasis.It significantlyinhibited LPS-induced DAG content,PKC activity and PKCζ translocation in aconcentration-dependent manner.The CCK receptor,especially the CCK-Areceptor,might play a major role in this process. | Shun-jiang XU Wei-juan GAO Bin CONG Chun-ling MA Shu-jin LI Yi-ling LING Zhen-yong GU Yu-xia YAO | 2005 | Acta Pharmacologica Sinica2005，26，12： | 6 |
| 14 | 八肽胆囊收缩素抑制脂多糖诱导急性肺损伤小鼠的炎症反应显示文摘目的探讨八肽胆囊收缩素(cholecystokinin octapeptide,CCK-8)对脂多糖(lipopo- lysaccharide,LPS)诱导急性肺损伤(acute lung injury,ALI)小鼠炎症反应的影响。方法复制LPS致ALI小鼠模型。实验动物随机分为生理盐水对照组、LPS组(腹腔注射LPS)、LPS+CCK-8组(注射LPS前30 min腹腔注射CCK-8)及CCK-8组(单独注射CCK-8)。用酶联免疫吸附法(ELISA)及逆转录-聚合酶链反应(PT-PCR)检测不同时间点各组小鼠血清、肺组织中白细胞介素-1β(IL-1β)、IL-6的含量及mRNA表达情况。观察各组肺组织光镜病理改变。结果腹腔注射LPS可成功复制ALI小鼠模型,肺组织病理显示,在LPS组12h时可见肺间质充血、水肿,大量炎性症细胞浸润,腹腔预注射CCK-8可明显改善肺组织病理变化;腹腔注射LPS可使小鼠血清及肺组织中IL-1β、IL-6表达增加,分别于注射后2h及4h达到高峰,预先注入CCK-8可显著抑制IL-1β、IL-6的表达。结论CCK-8可能通过抑制ALI小鼠IL-1β、IL-6的表达参与抗炎反应过程,从而减轻LPS诱导的ALI小鼠肺组织炎症反应。 | 倪志宇 丛军 李淑瑾 丛斌 闫玉仙 徐锦荣 高峰 韩冬艳 刘霞 | 2007 | 中国急救医学2007，27，4： | 6 |
| 15 | Expression and cell-specific localization of cholecystokinin receptors in rat lung显示文摘AIM: To eluddate whether CCK receptors exist in lung tissues and their precise cellular localization in the lung.METHODS: CCK-AR and CCK-BR mRNA expression and cellular distribution in the rat lung were detected by highly sensitive method of/n $I^J reverse transcription-polymerase chain reaction (RT-PCR) and conventional in situ hybridization.RESULTS: CCK-AR and CCK-BR gene positive signals were observed in bronchial epithelial cells, alveolar epithelial cells,pulmonary macrophages and vascular endothelial cells of the rats' lung by in sitv RT-PCR. The hybridization signals of CCK-AR were relatively faint. By in sitv hybridization,however, only the signals of CCK-BR but not CCK-AR were detected in the lung, and the positive staining was only found in vascular endothelial cells and macrophages.CONCLUSION: CCK-AR and CCK-BR gene were present in pulmonary vascular endothelial cells, macrophages, bronchial epithelial cells and alveolar epithelial cells, which play an important role in mediating the regulatory actions of CCK-8 on these cells. | Shu-JinLi Yi-LingLing Yu-XiaYao Zhen-YongGu Jun-XiaWang Hong-YuYou BinCong | 2003 | World Journal of Gastroenterology2003，9，6： | 6 |
| 16 | 八肽胆囊收缩素对经钥孔戚血蓝蛋白免疫小鼠T淋巴细胞亚群的影响显示文摘目的:探讨八肽胆囊收缩素(CCK-8)对经钥孔戚血蓝蛋白(KLH)免疫小鼠T淋巴细胞亚群的影响。方法:雌性BALB/c小鼠KLH免疫同时分别给予不同剂量CCK-8。流式细胞法检测小鼠外周血及脾细胞中CD4+、CD8+T细胞阳性百分率;RT-PCR法检测脾细胞中Th1型细胞因子IFN-γ、Th2型细胞因子IL-4 mRNA表达;ELISA法检测其培养上清中IFN-γ、IL-4水平;HE染色观察小鼠肺组织病理变化。结果:CCK-8下调KLH免疫小鼠外周血及脾细胞中上升的CD4+、CD8+T细胞阳性百分率,降低CD4+/CD8+比值;进一步提高其IFN-γ mRNA表达和培养上清中IFN-γ分泌量,同时下调上升的IL-4 mRNA表达和培养上清中IL-4分泌量;减轻KLH免疫所致小鼠肺部炎症。结论:CCK-8可调节适应性免疫应答,抑制T细胞尤其是CD4+T细胞活性;抑制Th2功能,提高Th1功能,因此可能在变态反应性疾病的发病和防治中具有一定作用。 | 宋宁 李淑瑾 丛斌 魏春华 丛军 张风华 马春玲 倪志宇 姚玉霞 | 2007 | 中国病理生理杂志2007，23，3： | 6 |
| 17 | 大鼠肠巨噬细胞TNFα表达及复方大承气汤的影响显示文摘目的:探讨体外培养的肠巨噬细胞分泌TNFα的规律及地塞米松、TNFα单克隆抗体及复方大承气汤对LPS诱导的肠巨噬细胞TNFα产生的影响。方法:体外分离培养大鼠肠巨噬细胞。设对照组、脂多糖组、地塞米松处理组、TNFα单抗处理组和复方大承气汤处理组.每组分别在3h,6h,12h和24h取上清液,用放免法检测TNFα浓度。并分别收集肠巨噬细胞,提取RNA,采用RT-PCR法相对定量TNFα mRNA。结果:肠巨噬细胞经脂多糖(LPS)诱导后,各时相TNFα分泌及TNFmRNA表达均明显增加;地塞米松、TNFα单克隆抗体及复方大承气汤处理后,各时相TNFα分泌都较脂多糖(LPS)诱导组显著下降,各处理组TNFα mRNA表达在3h时与脂多糖(LPS)诱导组比较无明显差异,6h、12h、24h,地塞米松、复方大承气汤处理组显著降低,而TNFα单克隆抗体处理组无明显差异。结论:LPS是肠巨噬细胞分泌TNFα的有效激活剂,地塞米松、复方大承气汤能从蛋白质及核酸水平抑制TNFα的产生,而TNFα单克隆抗体只能从蛋白质水平抑制TNFα的产生。 | 陈海龙 王辉 李文利 范琦 | 2003 | 世界华人消化杂志2003，11，4： | 6 |
| 18 | CCK-8对IL-1β诱导大鼠滑膜细胞株RSC-364增殖的影响显示文摘目的研究八肽胆囊收缩素(CCK-8)对IL-1β诱导大鼠滑膜细胞增殖的影响及相关机制。方法应用噻唑蓝(MTT)比色法检测CCK-8对IL-1β诱导RSC-364细胞增殖的影响;应用Westernblot检测CCK-8对IL-1β诱导RSC-364细胞p38MAPK磷酸化的影响。结果CCK-8剂量依赖性(10-12、10-10、10-8、10-6mol.L-1)抑制IL-1β诱导的RSC-364细胞增殖;CCK-8剂量依赖性(10-10、10-8、10-6mol.L-1)抑制了IL-1β诱导的RSC-364细胞p38MAPK的磷酸化;且CCK-8A、B受体拮抗剂CR1409或CR2945均减弱了CCK-8的抑制效应。结论CCK-8剂量依赖性抑制了IL-1β诱导的RSC-364细胞增殖,该作用由CCK-AR和CCK-BR介导,并可能通过抑制p38MAPK磷酸化而实现的。 | 韩冬艳 丛斌 徐锦荣 李淑瑾 马春玲 倪志宇 | 2006 | 中国药理学通报2006，22，9： | 5 |
| 19 | 脂多糖对大鼠肺间质巨噬细胞CCK受体mRNA表达的影响显示文摘目的:探讨胆囊收缩素(cholecystokinin,CCK)受体CCK—AR及CCK—BR mRNA在大鼠肺间质巨噬细胞(PIMs)内的表达及脂多糖(lipopolysaccharide,LPS)对其表达的影响。方法:用酶消化法结合肺泡灌洗和肺循环灌洗技术分离纯化大鼠PIMs,用LPS(10 mg/L)孵育PIMs 0.5-12 h。采用RT-PCR及Southern印迹技术观察CCK受体在大鼠PIMs内的表达亚型及LPS对其表达的影响。结果:经RT—PCR检测显示。CCK—AR和CCK—BR mRNA在大鼠PIMs均有表达,CCK—ARmRNA RT—PCR扩增产物为1.37 kb,CCK—BR mRNA RT—PCR扩增产物为480 bp。CCK—BR mRNA的相对表达量高于CCK—AR;LPS作用2 h可明显诱导2种CCK受体mRNA表达上调,至12 h仍维持较高水平。用γ-32P—ATP标记的两种特异性探针分别对CCK—AR和CCK—BR mRNA RT—PCR扩增产物进行Southern分子杂交,结果均有特异性杂交带出现。结论:肺间质巨噬细胞有CCK—AR和CCK—BR mRNA表达,LPS可诱导2种CCK受体mRNA表达上调。 | 许顺江 高维娟 姚玉霞 谷振勇 丛斌 | 2003 | 第二军医大学学报2003，24，11： | 5 |
| 20 | The mRNA expression patterns of tumor necrosis factor-a and TNFR-I in some vital organs after thermal injury显示文摘AIM: To investigate changes of tumor necrosis factor-α (TNFα) and TNFR-Ⅰ expression in vital organs and their significance in the pathogenesis of multiple organ damage associated with endogenous endotoxin following major burns.METHODS: Wistar rats subjected to a 35 % full-thickness scald injury were sacrificed at 12 h, 24 h, 48 h, and 72 h postburn, respectively. Meanwhile, eight rats were taken as normal controls. Tissue samples from liver, spleen, kidney,lung and intestine were collected to assay tissue endotoxin levels and measure TNF-α and TNFR-Ⅰ expression, In addition, blood samples were obtained for the determination of organ function parameters.RESULTS: Endotoxin levels in liver, spleen and lung increased markedly after thermal injury, with the highest level in liver. The gene expression of TNF-α in liver, lung and kidney was up-regulated after thermal injury, while the TNFR-Ⅰ mRNA expression in liver, lung, kidney and intestine was shown decreased throughout the observation period. Thus, the mRNA expression ratio of TNF-α to TNFRⅠ was significantly increased postburn, particularly in pulmonary tissue (67-fold). In addition, the significant correlations between the expression of TNFR-Ⅰ or the expression ratio of TNF-α/TNFR mRNA in liver tissue and serum aspartate aminotransferase levels were noted (P <0.05-0.01). Similar results were also obtained between pulmonary TNF-α mRNA expression and myeloperoxidase activities (P<0.01), whereas there was a highly negative correlation between levels of renal TNFR-Ⅰ mRNA expression and serum creatinine.CONCLUSION: Burn injury could result in the translocation of gut-derived endotoxin that was mainly distributed in the liver, spleen and lung. The translocated endotoxin then made the expression of TNF-α and TNFR-Ⅰ mRNA up-regulated and down-regulated respectively in various organs, which might be involved in the pathogenesis of multiple organ damage following burns. | Wen-Hui Fang Yong-Ming Yao Zhi-Guo Shi Yan Yu Ye Wu Lian-Rong Lu Zhi-Yong Sheng Department of Microbiology and Immunology,Burns Institute,304th Hospital of PLA,Beijing 100037,China | 2003 | World Journal of Gastroenterology2003，9，5： | 4 |
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