溃疡性结肠炎患者血清脂联素水平变化及意义

目的：检测溃疡性结肠炎（ulcerative colitis,UC）患者血清脂联素水平,探讨其临床意义。方法用酶联免疫吸附试验检测68例 UC 患者[根据严重程度分为轻度（n ＝23）、中度（n ＝24）和重度（n ＝19）;根据病变范围分为乙状结肠型（n ＝18）、左半结肠型（n ＝25）和全结肠型（n ＝25）]和20例健康体检者（对照组）血清脂联素水平,并分析其与 UC 临床特征的相关性。结果活动期 UC 患者血清脂联素水平显著高于缓解期 UC 患者和正常对照组（P ＜0．05）;重度 UC 患者脂联素水平与轻、中度比较,差异有统计学意义（P ＜0．05）;直乙结肠、左半结肠及全结肠 UC 患者血清脂联素水平与正常对照组比较,差异有统计学意义（P ＜0．05）。活动期 UC 患者血清脂联素水平与其疾病活动指数正相关（P ＜0．05）。结论脂联素可能参与 UC 疾病的发生发展。     

乌司他丁对溃疡性结肠炎患者血清炎症因子的影响

目的:观察乌司他丁对溃疡性结肠炎患者血清炎症因子的影响。方法:60例溃疡性结肠炎患者随机均分为观察组和试验组,同时选择20名健康志愿者作为健康对照组。试验组患者给予营养补充、维持水电解质平衡、5-氨基水杨酸等常规治疗;观察组患者在试验组治疗基础上加用乌司他丁20万U静脉注射,q12h。两组患者均以7 d为1个疗程,连续治疗2个疗程。观察两组患者治疗前后肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、IL-8、C反应蛋白(CRP)水平及结肠髓过氧化物酶(MPO)活性和病情活动指数(CAI)评分,并与健康对照组进行比较,同时记录不良反应发生情况。结果:两组患者治疗前后TNF-α、IL-1β、IL-8、CRP水平及MPO活性显著高于健康对照组,差异均有统计学意义(P<0.05)。治疗后,两组患者TNF-α、IL-1β水平和MPO活性、CAI评分及观察组IL-8、CRP水平显著低于同组治疗前,且观察组TNF-α、IL-8、CRP水平显著低于试验组,差异均有统计学意义(P<0.05)。两组患者均未见明显不良反应发生。结论:在常规治疗基础上加用乌司他丁可有效抑制溃疡性结肠炎患者多种血清炎症因子的表达,缓解结肠炎症反应与损伤,且安全性较好。     

利拉鲁肽对2型糖尿病患者血清炎症因子及脂联素的影响

目的:探讨利拉鲁肽对2型糖尿病患者血清炎症因子及脂联素的影响。方法:2型糖尿病患者60例(2015年1月~2016年1月),另外选择同期健康体检者60例,比较两组各项检测指标。结果:观察组和对照组的BMI、SBP、DBP、TC、TG无明显差异,P0.05;和对照组对比,观察组治疗前FPG、2hPG、HbA1c、IL-6、TNF-a、Hs-CRP、APN明显更高,P0.05;和治疗前对比,观察组治疗后FPG、2hPG、HbA1c、IL-6、TNF-a、Hs-CRP、APN明显上升,P0.05。结论:利拉鲁肽应用于2型糖尿病患者的治疗中,能够有效地降低血清炎症因子和脂联素水平,值得临床广泛应用以及推广。     

脂联素、肿瘤坏死因子-α与动脉粥样硬化的相关性

肿瘤坏死因子-α作为危险因子促进动脉粥样硬化的发生发展,而脂联素却是一个具有心血管保护作用的因子,它们相互作用参与了多个病理生理过程。     

脑梗死患者血清脂联素水平变化的相关性研究

目的分析脑梗死患者血清脂联素水平变化,探讨其临床意义。方法选取2014年1月至2015年1月我院确诊的脑梗死患者54例,并选取同期来我院检查,后证实为非脑梗死的正常健康者46例,其中脑梗死组再根据按NIHSS评分分为轻、中、重度组,分别动态检测两组1、3、7d不同时间点血清脂联素水平。结果脑梗死患者在不同时间点的血清脂联素水平较正常组均明显降低,差异有统计学意义(P<0.05)。随着脑梗死病变程度增加,各个同时间点患者血清脂联素水平随着病情的加重而降低,差异有统计学意义(P<0.05)。不同时间点脑梗死病变程度增加,血清脂联素水平呈递减趋势,差异有统计学意义(P<0.05)。结论对患者血液中血清脂联素水平的含量进行检测,对脑梗死的早期预防和诊断有较大的临床应用价值。     

血浆脂联素水平与冠心病的相关性

目的观察冠心病患者血浆脂联素水平,并探讨血浆脂联素水平与冠心病间的关系。方法经冠状动脉造影证实的冠心病患者共219例,对照组187例,采用Adiponectin ELISA试剂盒检测血浆脂联素水平,检测空腹血糖(BS)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C);计算体重指数。结果冠心病组患者的脂联素水平(6.3vs 12.6,P<0.01)显著低于对照组;Spearman偏相关分析显示经年龄、性别校正后脂联素水平与BS、SBP、LDL-C、TG呈负相关,与HDL-C呈正相关;多元logistic回归分析显示脂联素水平与冠心病及其主要危险因子独立相关。结论冠心病患者血浆脂联素水平降低,可能是冠心病的一个新的独立危险因子。     

糖尿病脂肪肝患者网膜素-1与脂联素、炎症因子关系研究

【摘要】目的研究2型糖尿病（T2DM）合并非酒精性脂肪性肝病（NAFLD）患者血浆网膜素-1与脂联素和肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、高敏C反应蛋白（hs-CRP）等炎症因子的关系。方法采用酶联免疫吸附法（ELISA）检测T2DM合并NAFLD组（A组,63例）、T2DM不合并NAFLD组（B组,63例）和正常对照组（C组,70例）的血浆网膜素-1和脂联素水平,同时测定上述3组生化指标及炎症指标（hs-CRP、TNF-α和IL-6）,应用相关分析和多元回归分析方法分析血浆网膜素-1与脂联素及炎症指标的关系,应用Logistic回归分析T2DM合并NAFLD的影响因素。结果A组血浆网膜素-1（27.02±2.82）μg/L、脂联素水平（11.98±3.63）mg/L低于B组[分别为（31.52±2.81）μg/L（15.85±3.28）mg/L]和C组[分别为（35.92±2.80）μg/L、（ 19.88±3.44）mg/L],且B组低于C组（P＜0.01）,A组血浆网膜素-1水平与脂联素、高密度脂蛋白胆固醇（HDL-C）正相关,与TNF-α、IL-6、空腹血（FBG）、胰岛素抵抗指数（HOMAIR）、内脏脂肪面积、腰围、腰臀比（WHR）、游离脂肪酸（FFA）负相关（P＜0.05或P＜0.01）;多元逐步线性回归分析表明脂联素、TNF-α、IL-6是血浆网膜素-1水平的影响因素。Logistic回归分析显示网膜素-1、hs-CRP、内脏脂肪面积及游离脂肪酸（FFA）是T2DM合并NAFLD的独立影响因素（P＜0.01）。结论 T2DM患者合并NAFLD与网膜素-1降低相关,网膜素-1表达可能会受到脂联素及炎症因子的影响。     

妊娠糖尿病患者血清脂联素水平变化及其与炎症因子和胰岛素抵抗的关系

目的探讨妊娠糖尿病(GDM)患者血清脂联素(APN)水平变化及其与炎症因子、胰岛素抵抗的关系。方法收集2009年7月至2011年12月在我院妇产科行常规产前检查的孕妇100名,根据糖耐量结果分为GDM45例,正常糖耐量组(NGT)55例,同时收集50名非妊娠健康育龄妇女作为对照组。使用酶联免疫吸附试验(ELISA)检测APN、白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α水平,免疫比浊法检测高敏C反应蛋白(hs-CRP)水平。结果与非妊娠对照组相比,妊娠期妇女血清IL-6、hs-CRP、TNF-α、空腹胰岛素(Fins)、甘油三酯(TG)水平及稳态胰岛素评估模型胰岛素抵抗(HOMA-IR)明显升高而APN水平明显降低(P<0.01或<0.05);GDM组血清IL-6、hs-CRP、TNF-α以及HOMA-IR又较NGT组显著升高,而APN水平则明显降低(均P<0.01)。在妊娠期妇女中,APN与hs-CRP、IL-6、TNF-α、TG水平及HOMA-IR呈负相关(r=-0.391、-0.373、-0.381、-0.352,-0.407,均P<0.01);在校正了年龄、孕周、体质量及胰岛素抵抗的影响后APN与hs-CRP、IL-6、TNF-α仍呈负相关(r=-0.322、-0.324、-0.314,均P<0.01)。结论 GDM患者APN水平明显降低,其可造成GDM患者炎症反应失衡,可能是导致GDM患者胰岛素抵抗的重要危险因素。     

血清脂联素水平与代谢综合征组分的相关性研究

目的探讨血清脂联素水平与代谢综合征(MS)各组分的相关性。方法采用整群随机抽样的方法,抽取齐齐哈尔市的两个城区,经调查和体检,筛选出MS患者235例。通过对MS患者的脂联素水平与MS各组分(腰围、血压、血糖、血脂)相关性分析及主成分回归分析,初步探讨血清脂联素水平与MS各组分的关系。结果男性脂联素水平为(2.82±1.73)μg/mL低于女性的(5.12±3.51)μg/mL,差异有统计学意义(Z=-5.25,P=0.00)。脂联素水平[(4.38±3.23)μg/mL与腹部肥胖相关,其与腰围[(93.37±7.76)cm]的Spearman秩相关系数为rs=-0.18(tr=-2.79,P=0.01);与腰臀比(0.91±0.05)的Spearman秩相关系数为rs=-0.28(tr=-4.44,P=0.00),而与人体质量指数(BMI)[(26.85±3.10)kg/m2]无显著相关性(rs=-0.10,tr=-1.45,P=0.15)。脂联素与胰岛素抵抗相关指标关系密切,包括空腹血糖[(5.48±1.72)mmol/L](rs=-0.13,tr=-2.00,P=0.05)、空腹胰岛素[(11.52±5.34)mU/L](rs=-0.15,tr=-2.31,P=0.02)、稳态模式评估法的胰岛素抵抗指数(HOMA-IR)(2.90±2.07)(rs=-0.17,tr=-2.63,P=0.01)及三酰甘油水平[(2.11±1.24)mmol/L](rs=-0.24,tr=-3.77,P=0.00)。脂联素与总胆固醇水平[(5.01±1.19)mmol/L](rs=-0.05,tr=-0.78,P=0.44)、高密度脂蛋白胆固醇(HDL-C)[(1.21±0.32)mmol/L](rs=0.06,tr=0.93,P=0.36)、收缩压[(131.40±14.93)mmHg,1mmHg=0.133kPa](rs=-0.02,tr=-0.34,P=0.73)及舒张压[(86.77±9.14)mmHg](rs=-0.02,tr=-0.27,P=0.78)无显著相关性。结论 MS患者血清脂联素水平与腹部肥胖及胰岛素抵抗相关指标呈负相关,而与血压未见直接联系。     

抗生素相关性结肠炎伴发溃疡性结肠炎的探讨

目的 观察抗生素相关性结肠炎伴发溃疡性结肠炎的临床特点及两者关系。方法 分析、总结7例(男3例,女4例;年龄48～83岁,平均66岁)确诊为抗生素相关性结肠炎同时伴发溃疡性结肠炎患者的临床资料、结肠镜报告、病理报告等,追踪其治疗效果。结果 7例患者既往无慢性腹泻病史;因原发病在较长时间内(6～20天,平均15天)接受1～3种广谱抗生素治疗后出现腹痛、腹泻、发热等症状;大便常规检查均见多量的粘液和红白细胞;大便细菌培养均为阴性;5例外周血白细胞显著升高、以中性粒细胞为主;结肠镜及病理检查可见特异的抗生素相关性结肠炎和溃疡性结肠炎表现;按抗生素相关性结肠炎治疗后,病情可得到控制,其中 3例需要使用柳氮磺胺吡啶(SASP)治疗,愈合良好。结论 抗生素相关性结肠炎可同时伴有溃疡性结肠炎发生,可能与它们有相似的发病机制有关。     

Murine models of ulcerative colitis

Ulcerative colitis (UC) is an inflammatory bowel disease of unknown etiology limited to the large intestine. The disease is prevalent in industrial societies and is associated with specific ethnic populations. A number of murine models, each focused on distinct aspects of the disease process, were developed over the past 20 years to further our understanding of the pathogenesis of UC. These models have been and remain our best resource for the study of the disorder as a result of their homology to human UC and the ease in which they can be manipulated and examined. This review examines and distills what has been leamed from these models and how this information is related back to human UC.     

Dextran sulfate sodium-induced ulcerative colitis leads to testicular toxicity in mice: Role of inflammation,oxidative stress and DNA damage

Ulcerative colitis is associated with an alteration in gonadal hormones and affects testicular weight in rodents. However, association of ulcerative colitis with testicular damage is not clearly known. Ulcerative colitis was induced using 5% (w/v) dextran sulfate sodium in normal drinking water for 1, 7-day cycle in short-term study and 2.5% (w/v) dextran sulfate sodium in normal drinking water for 4 cycles with 2 weeks remission period between each cycle in long-term study. Ulcerative colitis was associated with a significant increase in inflammation, oxidative stress, DNA damage in testes and sperm DNA damage and a significant decrease in the epididymal sperm count and 3β-HSD expression. No difference was observed in the plasma testosterone levels between control and treatment groups. In the present study, ulcerative colitis was associated with testicular damage, and juvenile mice were found to be more sensitive than adult mice.     

非酒精性脂肪性肝病患者血清脂联素与胰岛素表达水平及其相关性研究

目的 探讨非酒精性脂肪性肝病患者血清脂联素与胰岛素表达水平及其相关性.方法 选择2010年1月至2011年1月自贡市仁济医学中心收治的非酒精性脂肪性肝病患者50例为观察组,同时收集健康志愿者40例为对照组.用酶联免疫吸附测定法检测2组空腹及餐后2h血清脂联素水平,用化学发光法检测空腹及餐后2h胰岛素表达水平,并进行相关性分析.结果 观察组和正常对照组空腹脂联素水平分别为（912 ±29）、（1 033±53）μg/L,组间差异有统计学意义（P＜0.05）;空腹胰岛素水平分别为（13.8±1.0）、（7.3±1.0）mU/L,组间差异有统计学意义（P＜0.01）.观察组和正常对照组餐后2h脂联素水平分别为（854 ±38）、（1 010±48）μg/L,组间差异有统计学意义（P＜0.05）;餐后2h胰岛素水平分别为（112 ±23）、（28 ±3） μg/L,组间差异有统计学意义（P＜0.01）.相关性分析显示,非酒精性脂肪性肝病患者空腹及餐后2h脂联素与胰岛素水平均呈负相关（空腹：r=-0.328,P=0.020;餐后2 h：r=-0.391,P =0.005）.结论 非酒精性脂肪性肝病进展的同时伴随着胰岛素及脂联素水平的变化,二者呈负相关,这种负相关可能以餐后2h更明显.     

改良式保留灌肠法治疗溃疡性结肠炎

目的：观察改良式保留灌肠法治疗溃疡性结肠炎的效果。方法：将80例溃疡性结肠炎患者随机分为观察组（A组）40例和对照组（B组）40例。观察组采用药物中加入淀粉成糊状,使用一次性吸痰管代替肛管,采用缓慢推注替代滴注,同时配合体位调整的改良式保留灌肠法;对照组采用常规保留灌肠法。结果：观察组患者药物外溢少,保留时间长,治疗效果好。结论：改良式保留灌肠法可提高疗效,值得临床推广。     

溃疡性结肠炎联合治疗的临床观察

目的观察口服药物SASP结合药物灌肠联合治疗溃疡性结肠炎(UC)的疗效。方法 2009年1月至2011年3月期间该院收治住院的22例溃疡性结肠炎患者分为两组:联合治疗组11例,采用口服柳氮磺胺吡啶(SASP)+药物灌肠(思密达、地塞米松、庆大霉素)治疗;对照组11例,仅口服柳氮磺胺吡啶治疗。结果联合治疗组总有效率100.0%,对照组总有效率63.6%,两组比较差异有统计学意义(P<0.05)。结论口服药物结合药物灌肠联合治疗UC具有很好的疗效。     

美沙拉嗪治疗溃疡性结肠炎的疗效

目的 探讨美沙拉嗪治疗溃疡性结肠炎的临床疗效与安全性.方法 溃疡性结肠炎患者84例随机均分为两组,分别在支持治疗的基础上,观察组加用美沙拉嗪治疗,每日口服3次,1.0 g/次;对照组加用柳氮磺胺吡啶常规治疗;疗程为8周.比较两组临床疗效和治疗前后外周血C反应蛋白(CRP)、IL-6和TNF-α变化,记录治疗期的不良反应.结果 观察组的总有效率为97.6％,明显高于对照组的81.0％ (P＜0.05).治疗后两组外周血CRP和炎性细胞因子IL6和TNF-α水平均明显下降,且观察组的改变更为明显(P＜0.05).两组的不良反应发生率相仿(4.8％vs.9.5％)(P＞0.05).结论 美沙拉嗪治疗溃疡性结肠炎的临床疗效优于柳氮磺胺吡啶,能够明显改善患者体内的炎性状态.     

Berberine inhibits IFN-γ signaling pathway in DSS-induced ulcerative colitis

AimsThe potential signaling pathways and core genes in ulcerative colitis (UC) were investigated in this study. Furthermore, potential mechanisms of BBR in treating UC were also explored.MethodsExpression profiling by array of UC patients were obtained from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were determined with the differential analysis. The biological functions of DEGs were analyzed through the Database for Annotation, Visualization and Integrated Discovery (DAVID). The Gene Set Enrichment Analysis (GSEA) was applied to analyze the expression differences between two different phenotype sample sets. Dextran sulfate sodium (DSS) was applied to establish UC model of mice and lipopolysaccharide (LPS) was utilized to induce inflammatory damage of NCM460 cells. Therapeutic effects of berberine (BBR) on disease performance, pathologic changes and serum supernatant indices were analyzed in vivo. To further investigate the potential mechanisms of BBR in treating UC, the expression of genes and proteins in vivo and in vitro were examined by RT-qPCR, immunohistochemical staining and western blotting.ResultsImmune-inflammatory genes were identified and up-regulated significantly in UC patients. In addition, IFN-γ signaling pathway and its core genes were significantly up-regulated in the phenotype of UC. All disease performance and the pathologic changes of UC in mice were evidently ameliorated by BBR treatment. The pro-inflammatory cytokines of serum, including CXCL9, CXCL1, IL-17 and TNF-α, in UC mice were significantly reduced by treatment of BBR. In terms of mechanisms of BBR in treating UC, the pro-inflammatory and immune-related genes, encoding IFN-γ, IRF8, NF-κB and TNF-α decreased significantly in UC mice followed by BBR treatment. Meanwhile, the expression of IFN-γ and its initiated targets, including IRF8, Ifit1, Ifit3, IRF1, were suppressed significantly by BBR treatment in vivo. The blocking of IFN-γ in vitro led to the silence of IFN-γ signaling pathway after exposure to BBR. Furthermore, the blocking of IFN-γ in vitro led to the silence of IFN-γ signaling pathway after exposure to BBR.ConclusionBBR holds anti-inflammatory activity and can treat UC effectively. The anti-inflammatory property of BBR is tightly related to the suppression of IFN-γ signaling pathway, which is crucial in immune-inflammatory responses of the colon mucosa.     

LncRNA CDKN2B-AS1 relieved inflammation of ulcerative colitis via sponging miR-16 and miR-195

BackgroundThis study was aimed to explore the differential expression of lncRNA CDKN2B-AS1-miR-195-5p/miR-16-5p axis in ulcerative colitis (UC) and its role in regulating UC pathogenesis.MethodsOne hundred and eighty-seven UC patients and one hundred and fifty-two healthy volunteers were recruited, and their blood samples were collected. Inflammatory cytokines in serum were determined with ELISA, and lncRNA CDKN2B-AS1, miR-195-5p and miR-16-5p levels were detected with RT-PCR. Then pcDNA3.1-CDKN2B-AS1, si-CDKN2B-AS1, miR-195-5p mimic, miR-195-5p inhibitor, miR-16-5p mimic and miR-16-5p inhibitor were transfected into HT29 cells, and proliferation and apoptosis of the cells were assessed. Dual-luciferase reporter gene assay was implemented to identify the sponging relationship between lncRNA CDKN2B-AS1 and miR-195-5p/miR-16-5p.ResultsCDKN2B-AS1 level was negatively correlated with levels of inflammatory cytokines, including TNF-α, IL-6 and sIL-2R, yet miR-16-5p and miR-195-5p levels were negatively correlated with the CDKN2B-AS1 level. The CDKN2B-AS1 combined with miR-16-5p and miR-195-5p also achieved an optimum efficacy in differentiating between light and medium UC, light and severe UC, as well as medium and heavy UC. Furthermore, pcDNA3.1-CDKN2B-AS1 depressed expressions of IFN-γ, IL-8, IL-1β and TNF-α in HT29 cells (P < 0.05), and strengthened proliferation of the cells (P < 0.05). CDKN2B-AS1 also sponged and regulated miR-16-5p and miR-195-5p in HT29 cells, and miR-16-5p and miR-195-5p could reverse the effect of CDKN2B-AS1 on inflammatory cytokine production, barrier function and apoptosis of HT29 cells (P < 0.05).ConclusionLncRNA CDKN2B-AS1 regulated inflammation of UC by sponging miR-195-5p and miR-16-5p, providing an alternative for diagnosis and treatment of UC.