胶质细胞系源性神经营养因子对泻药性结肠大鼠肠道传输功能的影响

背景：慢传输型便秘（STC）患者长期依赖泻剂排便，导致泻药性结肠，部分患者最终需手术切除结肠。目的：探讨胶质细胞系源性神经营养因子（GDNF）对泻药性结肠大鼠肠道传输功能的影响。方法：以大黄灌胃建立大鼠STC模型。将大鼠随机分为正常NaCl组、正常GDNF组、模型NaCl组和模型GDNF组。正常GDNF组和模型GDNF组大鼠尾静脉注射GDNF，其余两组注射0．9％NaCl溶液。1周后处死大鼠，以墨汁推进试验测定肠道传输功能，并行结肠组织HE染色。结果：模型NaCl组肠道推进率显著低于正常NaCl组（P〈0．01）；模型GDNF组推进率显著高于模型NaCl组（P〈0．01）．结肠黏膜组织学表现较模型NaCl组有所改善。结论：外源性GDNF可明显改善大鼠肠道传输功能。     

非甾体抗炎药及其相关胃肠疾病

非甾体抗炎药（NSAIDs）具有解热、镇痛、抗炎等作用。随着NSAIDs临床应用的增多，其相关不良反应成为日益突出的问题．其中最常见的是胃肠道不良反应。本文从NSAIDs的作用机制出发，对NSAIDs相关胃肠疾病的发病机制和临床表现作一综述。     

慢传输型便秘发病机制的研究

慢传输型便秘(STC)的发病机制主要与肠神经系统(ENS)、Cajal间质细胞(ICC)、平滑肌、神经递质等有关。研究发现STC结肠组织中ENS出现退行性变化,肌间神经丛空泡变性,ICC数量减少,形态改变,平滑肌退行性变,多种神经递质发生改变。本文就STC发病机制的研究作一综述。     

非甾体类抗炎药与肠道损伤研究进展

非甾体类抗炎药（non—steroidal anti—inflammatory drug，NSAIDs）是一类具有抗炎、解热、镇痛等作用的药物，是目前全球使用最广泛的一类处方药，但长期大量使用，可引起各种毒副作用，尤以胃肠道损害最为常见。NSAIDs对胃十二指肠黏膜的损害已受到普遍关注，近年来随着内窥镜技术的不断提高，NSAIDs相关性肠黏膜的损害也开始受到人们的重视。本文就NSAIDs相关性肠道损伤文献作一综述。     

益气活血法对胃癌前病变大鼠血清细胞因子的影响

目的:观察益气活血法对胃癌前病变大鼠血清细胞因子的影响。方法:64只SD大鼠随机分为正常对照组8只和造模组56只,采用以MNNG损伤为主的综合法复制大鼠胃癌前病变模型,随机处死10只大鼠经病理确定造模成功后,再将46只造模组大鼠随机分为模型组12只、益气活血高、低剂量组各12只和胃复春组10只,分别给予益气活血方、胃复春混悬液灌胃治疗12周。ELISA法和放射免疫法测定大鼠血清TNF-α、IL-6和IL-8水平。结果:与正常对照组比较,模型组大鼠血清TNF-α、IL-6、IL-8水平较正常组降低,其中IL-8水平明显降低(P<0.01);药物治疗后与模型组比较益气活血高、低剂量组及胃复春组大鼠血清IL-6水平明显降低(P<0.01,P<0.05);胃复春组大鼠血清IL-8水平较益气活血高、低剂量组升高(P<0.05)。结论:益气活血法可改善胃癌前病变大鼠模型胃黏膜组织病理学,调节TNF-α和IL-6、IL-8水平可能是其防治胃癌前病变大鼠的作用机制之一。     

温郁金中新二萜类化合物C诱导人结肠腺癌SW620细胞凋亡的相关通路研究

目的探讨温郁金二萜类化合物C诱导人结肠腺癌SW620细胞凋亡的作用机制。方法以5-氟脲嘧啶(5-Flu-orouracil,5-FU)为阳性对照药物;采用噻唑蓝(methyl thia-zolyl tetrazolium,MTT)还原法检测化合物C和5-FU对SW620细胞增殖的影响;用流式细胞术(flow cytometry,FCM)检测两种药物诱导细胞凋亡的情况;用Western blot法检测化合物C作用后,细胞中ERK、p-ERK、JNK、p-JNK、p38、p-p38及caspase-3蛋白水平的变化。结果化合物C能抑制SW620细胞的增殖活性,并明显诱导细胞凋亡,其抑制率和凋亡率呈时间-浓度依赖性,且都明显高于5-FU组;其24、48和72 h的IC50分别为29.75、15.91和6.55 mg.L-1;化合物C能浓度依赖性地下调细胞中ERK、JNK、p38及其相应磷酸化蛋白的水平,并刺激caspase-3的蛋白表达。结论温郁金二萜类化合物C能抑制人结肠腺癌SW620细胞的生长并诱导凋亡,其作用机制可能与抑制MAPK信号转导通路、活化caspase-3有关。     

阿司匹林对胃肠黏膜的损伤作用

阿司匹林被广泛应用于心脑血管血栓性事件（心绞痛、心肌梗死、缺血性脑卒中等）的预防。然而,许多大型临床试验表明长期服用阿司匹林会引起胃肠黏膜损伤．即使低剂量阿司匹林亦会引起胃十二指肠黏膜损伤。本文就阿司匹林对胃肠黏膜的影响及其机制作一概述。     

抗肿瘤坏死因子α制剂治疗溃疡性结肠炎的荟萃分析

Objective To pool the data of studies and evaluate the efficacy and safety of TNFα blocking agents in the treatment of ulcerative colitis(UC).Methods The randomized clinical trials(RCT)that compared the efficacy or safety of TNFα in the treatment of UC were researched from Pubmed. OVID. EMBASE. Cochrane library, CNKI, Wanfang data and VIP Chinese Scientific and Technologic Periodical Database. Statistical heterogeneity between trials was evaluated by Revman 5.0 and was considered to exist when P＜0.1.Heterogeneity of the included articles was tested. which was used to select proper effect model to calculate. Publication bias was investigated through visual inspection of funnel plots. Results Nine RCT including 1226 cases were analyzed. Eight hundred and six cases had received TNFα treatment and 420cases had received placebo or glucocorticoid treatment. Compared with placebo or glucocorticoid groups, TNFα group achieved significantly higher rates of short-term clinical response, short-term clinical remission, long-term clinical response.10ng-term clinical remission and the total OR were 2.36(95%C,1.34-4.15),2.42(95%CI 1.22-4.81).3.22(95%CI2.28-4.55)and 2.82(95%CI1.91-4.16)respectively. TNFα group was less likely to undergo colectomy than placebo group and the total OR was 0.31(95%CI0.20-0.48).TNFα could not improve the mucosal healing and quality of lire. No significant difference was found in adverse effect between TNFα group and placebo or glueoeortieoid group(OR=1.07(95%CI0.55-2.09,P=0.84)).The rate of serious adverse effect in TNFα group was less than placebo or glueoeorticoid groups (OR=0.65,95%CI0.48-0.89,P=0.007).Inspection of the funnel plots for all dichotomous data measures had not revealed evidence of publication bias. Conclusions Patients with moderately to severely active UC treated with TNFαhave effective clinical response and clinical remission and are less likely to undergo colectomy than those receiving placebo or glucocorticoid. TNFα treatment is safe for UC but can not improve the mucosal healing and quality of life. Large-scale, high-quality RCTs ale needed to confirm or refuse the available evidence.     

抗肿瘤坏死因子α制剂治疗溃疡性结肠炎的荟萃分析

目的 根据现有临床研究评价抗TNFα制剂治疗溃疡性结肠炎(UC)的疗效与安全性.方法 检索Cochrane图书馆、EMBASE、PubMed、OVID数据库和中国知网、万方数据库、维普数据库中有关抗TNFa制剂[英夫利西单抗、阿达木单抗、塞妥珠单抗、依那西普、奥那西普、CDP571、CNI-1493、沙利度胺]治疗UC的RCT文献,采用Revman 5.0软件进行分析,并绘制漏斗图评定有无发表偏倚.结果 共9项RCT研究符合纳入标准,共包括1226例UC患者,其中806例接受抗TNFα制剂治疗,420例接受安慰剂或其他对照药物治疗.荟萃分析显示,在短期应答、短期缓解、长期应答、长期缓解方面,抗TNFα制剂明显优于对照组,OR值分别为2.36(95%CI 1.34～4.15)、2.42(95%CI 1.22～4.81)、3.22(95%CI 2.28～4.55)、2.82(95%CI 1.91～4.16).与对照组相比,抗TNFα制剂可以降低结肠切除率,OR值为0.31(95%CI 0.20～0.48);但在结肠黏膜愈合方面[OR值为1.59(95%CI 0.91～2.78)]及生活质量方面[炎症性肠病问卷(IBDQ)评分的加权均数差(WMD)为24.00(95%CI为-0.95～48.95)],两组的差异均无统计学意义.在安全性方面,两组不良反应发生率相似,OR值为1.07(95%CI0.55～2.09,P=0.84),但抗TNFα制剂的重度不良反应发生率明显低于对照组,OR值为0.65(95%CI 0.48～0.89).各计数资料观察指标的漏斗图均基本呈现下宽上窄、左右对称的图形,提示无发表偏倚.结论 抗TNFα制剂对于常规药物治疗无效的中、重度UC有较好的疗效,可以诱导UC短期应答,降低结肠切除率,并可维持长期的临床应答与临床缓解,严重不良反应的发生率较低,但抗TNFα制剂未能提高UC患者的生活质量与黏膜愈合率.

Abstract：

Objective To pool the data of studies and evaluate the efficacy and safety of TNFα blocking agents in the treatment of ulcerative colitis(UC).Methods The randomized clinical trials(RCT)that compared the efficacy or safety of TNFα in the treatment of UC were researched from Pubmed. OVID. EMBASE. Cochrane library, CNKI, Wanfang data and VIP Chinese Scientific and Technologic Periodical Database. Statistical heterogeneity between trials was evaluated by Revman 5.0 and was considered to exist when P＜0.1.Heterogeneity of the included articles was tested. which was used to select proper effect model to calculate. Publication bias was investigated through visual inspection of funnel plots. Results Nine RCT including 1226 cases were analyzed. Eight hundred and six cases had received TNFα treatment and 420cases had received placebo or glucocorticoid treatment. Compared with placebo or glucocorticoid groups, TNFα group achieved significantly higher rates of short-term clinical response, short-term clinical remission, long-term clinical response.10ng-term clinical remission and the total OR were 2.36(95%C,1.34-4.15),2.42(95%CI 1.22-4.81).3.22(95%CI2.28-4.55)and 2.82(95%CI1.91-4.16)respectively. TNFα group was less likely to undergo colectomy than placebo group and the total OR was 0.31(95%CI0.20-0.48).TNFα could not improve the mucosal healing and quality of lire. No significant difference was found in adverse effect between TNFα group and placebo or glueoeortieoid group(OR=1.07(95%CI0.55-2.09,P=0.84)).The rate of serious adverse effect in TNFα group was less than placebo or glueoeorticoid groups (OR=0.65,95%CI0.48-0.89,P=0.007).Inspection of the funnel plots for all dichotomous data measures had not revealed evidence of publication bias. Conclusions Patients with moderately to severely active UC treated with TNFαhave effective clinical response and clinical remission and are less likely to undergo colectomy than those receiving placebo or glucocorticoid. TNFα treatment is safe for UC but can not improve the mucosal healing and quality of life. Large-scale, high-quality RCTs ale needed to confirm or refuse the available evidence.     

肝性脊髓病1例报告并文献复习

肝性脊髓病（hepatic myelopathy,HM）又称门-腔分流性脊髓病,1949年由Leih和Cand首先报道,之后Zieve等再次对HM进行了详尽的描述,