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| 1 | 溃疡性结肠炎发病机制的研究进展显示文摘溃疡性结肠炎的发病机制较复杂,与多种因素联合作用有关。随着研究的进一步深入,目前认为集体免疫系统紊乱(如细胞因子、瘦素及脂联素等)起重要作用,此外还有遗传因素、环境因素和微生物感染等因素共同造成。了解溃疡性结肠炎的发病机制可为以后早期诊断、个体化治疗及预后评价提供线索,文章对其发病机制进行综述。 | 陈璐 周中银 | 2016 | 疑难病杂志2016，15，6： | 92 |
| 2 | 美沙拉嗪、柳氮磺胺吡啶对葡聚糖硫酸钠诱导的Balb/c小鼠急性溃疡性结肠炎的治疗和免疫影响显示文摘目的:探讨美沙拉嗪和柳氮磺胺吡啶对葡聚糖硫酸钠(DSS)致Balb/c小鼠急性溃疡性结肠炎的作用效果和对急性溃疡性结肠炎免疫功能的影响。方法:Balb/c小鼠给予3.5%DSS水溶液自由饮用7 d建立溃疡性结肠炎模型,通过测定小鼠DAI指数、脏器指数、血清IL-4、结肠组织匀浆液IL-8的表达水平和小鼠体内CD4^+细胞、CD8+细胞、CD4^+CD25^+细胞的变化,来评价两种药物对小鼠急性溃疡性结肠炎的作用。结果:给药治疗后,美沙拉嗪组和柳氮磺胺吡啶组的DAI评分和CMDI评分均降低(P<0.01或者P<0.05),小鼠症状缓解。结肠黏膜充血水肿减轻,且两种药物均能\有效抑制病灶部位炎细胞的浸润。与模型组相比,美沙拉嗪组和SASP组CD3^+细胞数增加,CD8^+细胞数明显上升,CD4^+CD25^+细胞占CD4^+细胞比例增加,血清中IL-4含量显著上升(P<0.01),组织中IL-8含量显著下降(P<0.01);而美沙拉嗪组CD4^+细胞数目略有增加,SASP组CD4^+细胞数增加比较明显。结论:美沙拉嗪和柳氮磺胺吡啶可减轻DSS诱导的UC小鼠稀便、血便症状;两种药物对UC疾病的治疗可能与提高CD4^+细胞水平和IL-4含量及上调CD8+细胞水平有关。 | 魏永凯 耿福能 赵微 刘衡 杨志斌 高鹏飞 巫秀美 李辉 | 2016 | 中国医院药学杂志2016，36，14： | 20 |
| 3 | CXC趋化因子受体2和白细胞介素-8在炎症性肠病患者中的表达及其意义显示文摘背景:CXC趋化因子受体2(CXCR2)为G蛋白耦联受体超家族成员,主要参与肿瘤生长、血管形成以及炎症性疾病的发病,有研究显示其参与炎症性肠病(IBD)发病,但相关作用仍未明确。研究表明白细胞介素-8(IL-8)与CXCR1和CXCR2的相互作用在IBD发病中发挥重要作用。目的:探讨CXCR2和IL-8在IBD患者中的表达及其意义。方法:纳入武汉大学中南医院2013年10月—2014年12月收治的活动期IBD患者121例,分为克罗恩病(CD)组和溃疡性结肠炎(UC)组,选取70例同期健康体检者作为正常对照(HC)组。采用real-time PCR检测外周血和肠黏膜组织IL-8和CXCR2 mRNA表达;采用蛋白质印迹法检测肠黏膜组织CXCR2蛋白表达。结果:UC组外周血IL-8 mRNA表达水平显著高于HC组(P=0.017);CD组、UC组和HC组外周血CXCR2 mRNA表达水平无明显差异(P=0.285)。CD组、UC组和HC组肠黏膜组织IL-8 mRNA表达水平无明显差异(P=0.206);CD组和UC组肠黏膜组织CXCR2 mRNA表达水平显著高于HC组(P=0.002;P<0.001),且UC组显著高于CD组(P=0.005)。UC组和CD组肠黏膜组织CXCR2蛋白表达水平高于HC组(P=0.049;P=0.080)。结论:IBD患者肠黏膜组织CXCR2 mRNA和蛋白表达均显著上调,且以UC患者为著,下调肠黏膜CXCR2表达可为治疗UC提供新靶点。IL-8主要在UC患者外周血中高表达,提示IL-8主要与UC发病相关。 | 朱锋 王晓兵 刘适 吴婷 夏冰 | 2016 | 胃肠病学2016，21，6： | 12 |
| 4 | 基于mTOR/p-S6K1探讨加味附子理中汤干预UC大鼠肠黏膜炎症反应的效应机制显示文摘目的:探讨加味附子理中汤治疗溃疡性结肠炎(UC)模型大鼠的疗效及相关作用机制。方法:选用72只雄性SD大鼠,分为正常组,模型组,柳氮磺胺嘧啶组(0.5 g·kg^-1),加味附子理中汤高、中、低剂量组(23.62,11.81,5.91 g·kg^-1)。运用2,4,6-三硝基苯磺酸(TNBS)-乙醇复合造模法复制UC大鼠模型,连续灌胃治疗2周,观察各组大鼠一般情况,大鼠麻醉后腹主动脉采血,取结肠组织。运用结肠黏膜损伤指数(CMDI)半定量评分,苏木素-伊红(HE)染色观察大鼠结肠组织病理学改变,酶联免疫吸附测定(ELISA)检测大鼠血清白细胞介素(IL)-4,IL-6,IL-10,肿瘤坏死因子-α(TNF-α)含量;免疫组化和蛋白免疫印迹法(Western blot)分别检测结肠黏膜组织哺乳动物雷帕霉素靶蛋白(mTOR)及磷酸化核糖体蛋白S6激酶1(p-S6K1)蛋白表达。结果:与正常组比较,模型组大鼠CMDI评分显著升高(P<0.01),血清IL-4,IL-10含量显著下降,IL-6,TNF-α含量显著上升(P<0.01),结肠黏膜组织mTOR,p-S6K1蛋白表达水平显著上调(P<0.01);与模型组比较,加味附子理中汤高剂量组大鼠CMDI评分明显下降(P<0.05),高、中剂量组大鼠血清促炎因子IL-6,TNF-α显著降低(P<0.01),抗炎因子IL-4,IL-10明显升高(P<0.05,P<0.01);加味附子理中汤高剂量大鼠mTOR,p-S6K1的蛋白表达水平明显下调(P<0.05,P<0.01)。结论:加味附子理中汤高剂量组可显著减轻UC结肠黏膜充血水肿、炎性细胞浸润、腺体扭曲、排列紊乱等病理表现,其机制可能与其下调mTOR/p-S6K1信号、调控炎症因子的分泌有关。 | 郝彦伟 张怡 周雪雷 喻俊榕 曾进浩 郭宇 | 2020 | 中国实验方剂学杂志2020，26，13： | 12 |
| 5 | 四君子汤抗大鼠溃疡性结肠炎及对结肠组织GABA受体表达的影响显示文摘目的:研究四君子汤(Sijunzi decoctum,SJZD)对3%葡聚糖硫酸钠5000(dextran sulphate sodium,DSS)诱导的大鼠实验性溃疡性结肠炎的保护作用及对结肠组织GABA含量及其受体表达的影响.方法:40只♂Wistar大鼠随机分为正常组、模型组、SJZD低剂量(5.0 g/kg)组、SJZD中剂量(10.0 g/kg)组、SJZD高剂量(30.0 g/kg)组,正常组正常饮食蒸馏水,其余各组先以3%D S S诱导7 d建立大鼠溃疡性结肠炎模型,后SJZD组按照不同剂量(5.0、10.0、30.0 g/kg)灌胃给予SJZD,每天观察大鼠疾病活动指数(disease active index,DAI)评分.2 wk后处死所有动物,分离结肠,行结肠组织损伤程度(colon macroscopic damage index,CMDI)评分.ELISA法测量血清白介素1β(interleukin-1β,IL-1β)、I L-4水平,结肠组织匀浆测定超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)含量,HE染色镜下观察病理变化,免疫组织化学法SP法检测病变组织GABA A受体、GABA B受体的表达水平.结果:模型组动物结肠组织溃疡形成,伴有大量炎性细胞浸润及充血、间质水肿等明显病理变化,SJZD摄入不同剂量可不同程度的改善病变,模型组大鼠DAI、CMDI评分、血清I L-1β水平、组织匀浆M D A含量、结肠组织G A B A A受体表达与正常比较均有明显升高(P<0.01);S J Z D低、中、高剂量组上述各项指标亦明显增高;模型组、SJZD低、中、高剂量组血清IL-4水平,组织匀浆SOD含量与正常比较则明显降低(P<0.01);各实验组结肠组织GABA B受体表达与正常比较无明显差异(P>0.05).与模型组比较,SJZD中、高剂量摄入可有效逆转上述变化,以高剂量组差异最为明显.SJZD低剂量组在血清IL-1β、IL-4水平,DAI、CMDI评分及GABA A受体、GABA B受体的表达水平几方面与模型组比较差异并无统计学意义(P>0.05).各实验组结肠组织GABA B受体表达与模型组比较差异无统计学意义(P>0.05).结论:四君子汤可以明显改善DSS诱导的溃疡性结肠炎大鼠的炎症反应,其作用机制可能与改善抗氧化自由基以及细胞因子水平有关;GABA主要通过其GABA A受体参与溃疡性结肠炎的病理生理过程,四君子汤可明显影响GABA A受体表达水平. | 张燕翔 鲁兵 张恒文 余万桂 | 2014 | 世界华人消化杂志2014，22，34： | 9 |
| 6 | Norisoboldine, a natural aryl hydrocarbon receptor agonist, alleviates TNBS-induced colitis in mice, by inhibiting the activation of NLRP3 inflammasome显示文摘Although the etiology of inflammatory bowel disease is still uncertain, increasing evidence indicates that the excessive activation of NLRP3 inflammasome plays a major role. Norisoboldine(NOR), an alkaloid isolated from Radix Linderae, has previously been demonstrated to inhibit inflammation and IL-1β production. The present study was to examine the effect of NOR on colitis and the underlying mechanism related to NLRP3 inflammasome activation. Our results showed that NOR alleviated colitis symptom in mice induced by 2, 4, 6-trinitrobenzene sulfonic acid(TNBS). Moreover, it significantly reduced expressions of cleaved IL-1β, NLRP3 and cleaved Caspase-1 but not ASC in colons of mice. In THP-1 cells, NOR suppressed the expressions of NLRP3, cleaved Caspase-1 and cleaved IL-1β but not ASC induced by lipopolysaccharide(LPS) and adenosine triphosphate(ATP). Furthermore, NOR could activate aryl hydrocarbon receptor(AhR) in THP-1 cells, inducing CYP1 A1 mR NA expression, and promoting dissociation of Ah R/HSP90 complexes, association of AhR and ARNT, Ah R nuclear translocation, XRE reporter activity and binding activity of Ah R/ARNT/XRE. Both siA hR and α-naphthoflavone(α-NF) markedly diminished the inhibition of NOR on NLRP3 inflammasome activation. In addition, NOR elevated Nrf2 level and reduced ROS level in LPS-and ATP-stimulated THP-1 cells, which was reversed by either si AhR or α-NF treatment. Finally, correlations between activation of AhR and attenuation of colitis, inhibition of NLRP3 inflammasome activation and up-regulation of Nrf2 level in colons were validated in mice with TNBS-induced colitis. Taken together, NOR ameliorated TNBS-induced colitis in mice through inhibiting NLRP3 inflammasome activation via regulating AhR/Nrf2/ROS signaling pathway. | LV Qi WANG Kai QIAO Si-Miao DAI Yue WEI Zhi-Feng | 2018 | Chinese Journal of Natural Medicines2018，16，3： | 8 |
| 7 | 溃疡性结肠炎中医症候类型与Madcam-1、TNF-a及IL-8的相关性研究显示文摘目的:探讨溃疡性结肠炎(Ulcerative Colitis,UC)中医症候类型与患者血清中黏膜地址素粘附分子1(Madcam1)、肿瘤坏死因子-α(TNF-α)及白介素-8(IL-8)表达水平的相关性,为UC的临床症候分型及分证论治提供依据。方法:通过收集南通市中医院门诊及住院的UC患者108例,同时选择20例正常人作为对照。观察UC患者临床表现及肠镜下结肠黏膜的病理形态,判断其病情的轻重。对收集的UC患者进行症候分型,分为大肠湿热证,脾虚湿热证,肝郁气滞证,寒热错杂证,脾肾阳虚证。采用双抗体夹心ELISA法检测各组UC患者血清中Madcam-1,TNF-a和IL-8的表达水平。通过统计学分析,探讨各项指标与UC症候类型的相关性。结果:中重度UC患者血清中IL-8、TNF-α、Madcam1蛋白水平明显高于轻度患者与正常人群,具有明显的相关性。大肠湿热证与脾虚湿热证UC患者血清中IL-8、TNF-α、Madcam1蛋白水平明显高于其他组与正常人群,具有明显的相关性。结论:检测UC患者血清中Madcam-1,TNF-a及IL-8的表达水平,可作为判断UC病情轻重及临床症候类型的依据,抗Madcam-1,TNF-a及IL-8抗体可能是治疗UC的有效方法。 | 景姗 邵荣世 李卫兵 顾庆华 | 2017 | 四川中医2017，35，8： | 7 |
| 8 | 成人隐匿性自身免疫性糖尿病与溃疡性结肠炎患者外周血T细胞亚群失衡的临床意义显示文摘目的探讨LADA与溃疡性结肠炎(UC)患者外周血T细胞亚群变化及淋巴细胞失衡的临床意义。方法选取LADA、UC组各52例和健康对照(NC)组52名,采用单克隆抗体间接免疫荧光技术检测各组外周血淋巴细胞CD3+、CD4+、CD8+亚群百分比。结果 LADA、UC、NC组CD3+亚群比较差异均无统计学意义[(62.29±4.97)%vs(63.49±5.12)%vs(61.37±4.83)%,P>0.05]。UC组CD4+亚群较LADA、NC组降低[(27.63±6.85)%vs(35.87±5.92)%,P<0.01;(27.63±6.85)%vs(34.63±5.39)%,P<0.01]。LADA组CD8+亚群较UC、NC组升高[(27.54±3.05)%vs(22.21±3.46)%,P<0.01;(27.54±3.05)%vs(21.82±3.77)%,P<0.01]。LADA、UC组CD4+/CD8+较NC组降低[(1.35±0.37)vs(1.78±0.44),P<0.01;(1.32±0.51)vs(1.78±0.44),P<0.01]。结论 LADA、UC患者均出现淋巴细胞CD4+、CD8+亚群失衡,淋巴细胞亚群失衡参与两者发病,但具体机制不同。 | 杨德生 康玉华 索智敏 李福春 胡军红 陈宏超 庞妩燕 | 2014 | 中国糖尿病杂志2014，22，9： | 6 |
| 9 | Intestinal anti-inflammatory activity of Ground Cherry(Physalis angulata L.)standardized CO2 phytopharmaceutical preparation显示文摘AIM To investigate the effects of Ground Cherry(Physalis angulata L.)standardized supercritical CO_2 extract in trinitrobenzenesulphonic acid(TNBS)model of rat intestinal inflammation.METHODS The animals were divided into groups that received vehicle or P.angulata extract(PACO_2)orally at the doses 25,50 and 100 mg/kg daily by 5 d before TNBS damage.Protective effects of PACO_2 were assessed by macroscopic analysis,biochemical determinations of the levels of myeloperoxidase(MPO),alkaline phosphatase(ALP),glutathione and cytokines(such as INF-γ,IL-1β,IL-6,IL-10 and TNF-α),gene expression evaluation(including Hsp70,heparanase,NF-κB,mitogenactivated protein kinases(Mapk)1,3,6 and 9,and the mucins genes Muc 1,2,3 and 4)and histopathological studies using optical,and electronic(transmission and scanning)microscopy.RESULTS PACO2 extract promoted a significant reduction in MPO and ALP activities,reducing oxidative stress and neutrophil infiltration.These effects were accompanied by significant reduction of colonic levels of IFN-γand IL-6 and down-regulation of heparanase,Hsp70,Mapk3,Mapk9,Muc1 and Muc2 genes expression when compared with TNBS-control animals.In addition,protective effects were also evidenced by reduced neutrophil infiltration,recovery of cell architecture and replacement of mucin by histopathological and ultrastructural analysis.CONCLUSION Physalis angulata supercritical CO2 extract is an intestinal anti-inflammatory product that modulates oxidative stress,immune response and expression of inflammatory mediators,with potentially utility for treating inflammatory bowel disease. | luiz domingues almeida junior ana elisa valencise quaglio celso acácio rodrigues de almeida costa Luiz Claudio Di Stasi | 2017 | World Journal of Gastroenterology2017，23，24： | 4 |
| 10 | 氯丙嗪致大鼠便秘与炎性细胞因子表达的对照研究显示文摘目的探讨氯丙嗪应用对大鼠肠道炎症反应以及排便习惯的作用及相关机制。方法 50只SD雄性大鼠随机分为正常对照组,氯丙嗪低中高剂量组,以及氯丙嗪联合新斯的明给药共五组,灌胃氯丙嗪两周以后,考察氯丙嗪对大鼠排便习惯以及肠推动力的影响;分离提取结肠组织,采用酶联免疫反应以及Western blotting考察氯丙嗪对前炎性因子,炎性介质以及诱导型一氧化氮(NO)合酶(i NOS)、环氧合酶-2(COX-2)以及核转录因子(NF-κB)表达的作用。结果灌胃氯丙嗪(40 mg/kg)两周以后,与正常对照组相比,大鼠排便数量以及粪便含水量分别从(81±15)%,(60±13)%下降至(33±21)%,(25±27)%(P均<0.05),分离的大鼠结肠i NOS,COX-2以及NF-κB分别从(100±11)%,(100±9)%,(100±12)%增加至(289±19)%、(311±28)%、(209±18)%(P均<0.05),同时伴随着结肠中相关细胞因子以及炎性介质的增加。结论氯丙嗪长期使用,可使NF-κB活化,继而激活i NOS和COX-2,前炎性因子以及炎性介质进一步高表达,导致结肠炎症。 | 张家瑞 任丽娜 赵均铭 张勇 | 2015 | 四川精神卫生2015，28，2： | 1 |
| 11 | Longitudinal analysis of inflammation and microbiota dynamics in a model of mild chronic dextran sulfate sodium-induced colitis in mice显示文摘AIM:To characterize longitudinally the inflammation and the gut microbiota dynamics in a mouse model of dextran sulfate sodium(DSS)-induced colitis.METHODS:In animal models,the most common method used to trigger colitis is based on the oral administration of the sulfated polysaccharides DSS.The murine DSS colitis model has been widely adopted to induce severe acute,chronic or semi-chronic colitis,and has been validated as an important model for the translation of mice data to human inflammatory bowel disease(IBD).However,it is now clear that models characterized by mild intestinal damage are more accurate for studying the effects of therapeutic agents.For this reason,we have developed a murine model of mild colitis to study longitudinally the inflammation and microbiota dynamics during the intestinal repair processes,and to obtain data suitable to support the recovery of gut microbiota-host homeostasis.RESULTS:All plasma cytokines evaluated,except IL-17,began to increase(P<0.05),after 7 d of DSS administration.IL-17 only began to increase 4 d after DSS withdrawal.IL-1βand IL-17 continue to increase during the recovery phase,even when clinical signs of colitis had disappeared.IL-6,IL-10 and IFN-γreached their maxima 4 d after DSS withdrawal and decreased during the late recovery phase.TNFαreached a peak(a three-fold increase,P<0.05),after which it slightly decreased,only to increase again close to the end of the recovery phase.DSS administration induced profound and rapid changes in the mice gut microbiota.After 3 d of DSS administration,we observed a major reduction in Bacteroidetes/Prevotella and a corresponding increase in Bacillaceae,with respect to control mice.In particular,Bacteroidetes/Prevotella decreased from a relative abundance of 59.42%-33.05%,while Bacillaceae showed a concomitant increase from 2.77%to 10.52%.Gut microbiota rapidly shifted toward a healthy profile during the recovery phase and returned normal 4 d after DSS withdrawal.Cyclooxygenase 2 expression started to increase 4 d after DSS withdrawal(P<0.05),when dysbiosis had recovered,and continued to increase during the recovery phase.Taken together,these data indicated that a chronic phase of intestinal inflammation,characterized by the absence of dysbiosis,could be obtained in mice using a single DSS cycle.CONCLUSION:Dysbiosis contributes to the local and systemic inflammation that occurs in the DSS model of colitis;however,chronic bowel inflammation is maintained even after recovery from dysbiosis. | Luigia De Fazio Elena Cavazza Enzo Spisni Antonio Strillacci Manuela Centanni Marco Candela Chiara Praticò Massimo Campieri Chiara Ricci Maria Chiara Valerii | 2014 | World Journal of Gastroenterology2014，20，8： | 1 |
| 12 | 重组KGF-2突变体对TNBS诱导的复发性大鼠炎性肠病模型治疗作用的研究显示文摘目的制备复发性大鼠炎性肠病模型,评价重组KGF-2突变体(STEA)给药对2,4,6-三硝基苯磺酸(TNBS)诱导的复发性大鼠炎性肠病模型的治疗效果。方法利用2%的TNBS(100mg/kg)对雄性Wistar大鼠进行灌肠,3周后,再次利用TNBS(10毫克/只)处理这些大鼠。于再次灌肠当天,治疗组的大鼠腹腔注射3mg/kg STEA,模型对照组和正常组注射等量的PB缓冲液,每天1次,连续7天。对各组大鼠的生存状态、血清中IL-6和IL-1β的表达水平、以及结肠组织病理变化等情况进行观察和分析。结果利用TNBS二次致敏的方法,成功制备了复发性大鼠炎性肠病模型。STEA给药能显著降低模型大鼠血清中IL-6和IL-1β的表达水平,提高大鼠的存活率,促进受损结肠黏膜的修复。结论 STEA对TNBS诱导的复发性大鼠的结肠损伤具有治疗作用。 | 王金凤 王园园 付文亮 蔡欣 邹民吉 邢微微 陈惠华 徐东刚 | 2013 | 医学研究杂志2013，42，7： | 0 |
| 13 | Nilotinib-mediated mucosal healing in a rat model of colitis显示文摘AIM:To investigate the effects of nilotinib in a rat model of trinitrobenzene sulfonic acid(TNBS)-induced colitis.METHODS:Twenty-one Wistar albino female rats obtained from Dokuz Eylul University Department of Laboratory Animal Science were categorized into a control(n=7),TNBS(n=7)and nilotinib group(n=7).Saline was administered orally for 14 d to the control and the TNBS group.The TNBS group received rectal TNBS on the first day while saline was administered to the control group.The nilotinib group received 20mg/kg nilotinib for 14 d in 2 divided doses,starting the same day as TNBS administration.For 14 d,the rats were fed a standard diet,and their weights were recorded daily.After sacrifice,colon tissue samples from each group were scored for macroscopic and microscopic pathology.Apoptotic indices were determined by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method.Platelet-derived growth factor receptor(PDGFR)alpha and beta levels were assessed through immunohistochemistry staining scores and compared among the groups.Tissue and serum tumor necrosis factor(TNF)alpha levels were determined by enzyme-linked immunosorbent assay.RESULTS:Between days 1 and 14,the nilotinib group rats lost significantly less weight than the TNBS group rats(-0.7 g vs-14.0 g,P=0.047).The difference in weight between the control and nilotinib groups was also statistically significant(+8.3 gvs-0.7 g,P=0.031).From day 7 to day 14,the weight differences of the control group vs the TNBS group,the TNBS group vs the nilotinib group,and the control group vs the nilotinib group were all statistically significant(+8.0 g vs-11.1 g,P=0.007;-11.1 g vs+2.9 g,P=0.015;+8.0g vs+2.9 g,P=0.042,respectively).Macroscopic and microscopic scores were significantly lower in the nilotinib group than in the TNBS group(0.00±0.00 vs 1.43±0.65,P=0.009;2.86±0.55 vs 7.71±1.48,P=0.030,respectively).However,these scores were similar between the nilotinib and control groups.While no significant difference for the nilotinib vs control groups could be determined for PDGFR alpha and beta scores,PDGFR alpha and beta scores were lower in the nilotinib group than in the TNBS group.Furthermore,the TNF alpha levels in the serum,tissue and apoptosis scores were similar between the nilotinib and TNBS groups.CONCLUSION:Nilotinib prevents weight loss,facilitates mucosal healing by improving the pathological scores without introducing variation into the apoptotic scores or TNF alpha levels. | Pinar Ataca Mujde Soyturk Meral Karaman Mehtat Unlu Ozgul Sagol Gozde Dervis Hakim Osman Yilmaz | 2013 | World Journal of Gastroenterology2013，19，37： | 0 |
| 14 | NFSF15基因多态性与克罗恩病易患性的Meta分析显示文摘目的探讨NFSF15基因rs3810936多态性与克罗恩病(CD)易患性的关系。方法计算机检索数据库,收集有关NFSF15基因rs3810936多态性与CD易患性病例对照研究,提取纳入文献的相关数据进行Meta分析,以病例组与对照组NFSF15基因rs3810936位点基因模型的比值比(OR)为效应指标,漏斗图检测发表偏倚。结果共5篇研究符合纳入标准,累计病例1178例,对照1550例。Meta分析表明,NFSF15基因rs3810936多态性与CD易患性相关[纯合子比较模型(CCvsTr):OR:0.34,95%C10.17~0.72,P=0.004;杂合子比较模型(TCvsTT):OR=0.62,95%C10.54~0.72,P〈0.01;显性遗传模型(CC+TCvs1Tr):OR=2.18,95%C11.19~4.02,P=0.01;隐性遗传模型(CCVSTC+Tr):0R=0.46,95%C10.25~0.84,P=0.01]。结论NFSF15基因rs3810936多态性与CD易患性有明显关联性。 | 邓银芝 张长江 贺建华 | 2014 | 医学综述2014，20，12： | 0 |
| 15 | IL-12B基因多态性及单倍型与克罗恩病的关系研究显示文摘目的 探讨IL-12B基因多态性及单倍型与克罗恩病(CD)的关系。方法 选取94例CD患者(CD组)和106例健康体检者(对照组),采用改良多重高温连接酶检测反应技术检测IL-12B基因2个功能性单核苷酸多态性(SNP)位点rs3212227和rs6887695的等位基因及基因型,用Haploview 4.2软件进行连锁不平衡和单倍型分析,并分析IL-12B基因多态性及单倍型与CD的关系。结果 CD组与对照组比较,该2个IL-12B基因SNP位点的突变等位基因和基因型频率均无统计学差异(均P>0.05)。进一步亚组分析发现回肠型CD组患者rs6887695位点的突变C等位基因和GC+CC基因型频率均明显低于与对照组(28.75%vs 44.34%,P<0.05,OR=0.507,95%CI:0.291~0.882;50.00%vs 71.70%,P<0.05,OR=0.395,95%CI:0.186~0.836);而上述2个位点的等位基因及基因型频率分布在结肠病变(结肠型+回结肠型)CD组患者与对照组间比较均无统计学差异(均P>0.05)。此外,CD患者组内分层比较发现,与结肠病变CD组比较,回肠型CD组患者rs6887695位点的突变C等位基因、GC+CC基因型以及CC基因型频率亦均明显降低(28.75%vs 50.00%,P<0.05,OR=0.404,95%CI:0.218~0.745;50.00%vs 72.22%,P<0.05,OR=0.385,95%CI:0.163~0.908;7.50%vs27.78%,P<0.05,OR=0.150,95%CI:0.037~0.613)。经Haploview 4.2软件分析发现rs3212227和rs6887695 2个SNP位点之间存在中等强度连锁不平衡关系(D′=0.545,r2=0.235),但CD组与对照组比较,各单倍型的频率均无统计学差异(均P>0.05)。结论 IL-12B基因rs6887695位点多态性与CD的临床表型相关,该位点基因突变后可能降低回肠型CD的发病风险。 | 郭茂东 王群英 陈燕萍 滕卫军 马拥军 杨小云 韦炜 丁进 | 2018 | 浙江医学2018，40，9： | 0 |
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