缬草波春对肠易激综合征大鼠结肠GABABR表达的影响

目的 探讨缬草波春(valepotriats)对肠易激综合征(irritable bowel syndrome,IBS)大鼠结肠组织γ-氨基丁酸B型受体(Gamma-aminobutyric acid B recepter,GABABR)表达的影响及其意义.方法 Wistar大鼠32只,体重(360±20) g,将其随机分为正常组、模型组、缬草组、吗啡组,每组8只.应用正丁酸钠溶液灌肠法建立IBS大鼠模型,利用生理信号仪记录大鼠结肠张力-运动曲线,分析缬草波春对大鼠结肠运动的影响;用免疫组织化学方法检测大鼠结肠GABABR的表达.结果 模型组结肠运动平均张力显著高于正常组(P＜0.01),缬草组显著低于模型组(P＜0.01);模型组结肠肌间神经丛GABABR表达低于正常组 (P＜0.05),缬草组结肠肌间神经丛GABABR表达较正常组和模型组均明显增高(P＜0.01).结论 缬草波春可以降低结肠运动平均张力,解除结肠平滑肌痉挛,缓解IBS,机制可能与GABABR介导的调节有关.     

正丁酸盐诱导的大鼠非炎症性结肠致敏模型

目的: 研究正丁酸盐结肠灌注对大鼠结肠敏感性的影响, 探讨结肠致敏模型制作的新方法.方法: Wistar大鼠每天接受浓度为300 mmol/L丁酸盐1 mL从肛门灌肠2次, 共6 d. 分别在造模3、6 d后以半定量的方法观察大鼠对直肠扩张(CRD)的反应, 进行结肠敏感性评估, 记录初始感觉压力和最大耐受压力. 实验后处死大鼠, 取距肛门10 cm的结直肠, 观察肠黏膜损伤指数, 病理检查观察组织病理改变.结果: 模型组和盐水对照组均未见黏膜及黏膜下层组织结构破坏, 黏膜下嗜酸性粒细胞计数、肥大细胞计数无显著差异. 造模6 d模型组结肠运动最大压力较盐水对照组明显升高,差异有显著意义( t = 9.25, P<0.01). 模型组初始压力感觉及最大耐受压力较盐水对照组明显降低, 差异有显著意义( t = 36.71, 15.02, 均P<0.01).结论: 正丁酸盐灌肠可以使结肠敏感性增加,不破坏结肠黏膜组织结构, 结肠黏膜致敏与肥大细胞无关.     

缬草波春诱导MKN-45胃癌细胞凋亡

目的:研究缬草波春诱导胃癌细胞凋亡,探讨其诱导凋亡与半胱氨酸酶(Caspase)及生存素(Survivin)mRNA、P53蛋白、Survivin蛋白表达的关系.方法:以100 mg/L的缬草波春作用于加Caspase-3抑制剂、Caspase-8抑制剂、Caspase-9抑制剂和未加Caspases抑制剂培养的MKN-45细胞24,48和72 h,用流式细胞仪分别检测细胞凋亡率;不同浓度的缬草波春(5,10,25,50,100 mg/L)作用MKN-45细胞不同时间(24,48,72 h)后,用tripure提取液提取细胞RNA,用RT-PCR法,检测Survivin mRNA的表达.不同浓度缬草波春(50和100 mg/L)作用MKN-45胃癌细胞株24 h后,用免疫组化的方法,检测P53蛋白和Survivin蛋白的表达.结果:单用Caspase抑制剂组,作用24,48和72 h对MKN-45细胞凋亡率无明显影响,与对照组比较差异无显著意义.Caspase-3抑制剂、Caspase-9抑制剂与缬草波春联合应用后24,48和72 h使MKN-45细胞凋亡率高于对照组(24 h:5.73%,5.41% vs 4.38%,P＜0.01;48 h:6.88%,6.32% vs 4.35%,P＜0.01;72 h:7.72%,8.62% vs 4.54%,P＜0.01),低于缬草波春组(24 h:5.73%,5.41% vs 8.14%,P＜0.01;48 h:6.88%,6.32% vs 12.31%,P＜0.01;72 h:7.72%,8.62% vs 26.41%,P＜0.01),与对照组及缬草波春组比较差异均有显著意义(P＜0.01).Caspase-8抑制剂与缬草波春联合应用后24,48和72 h MKN-45细胞凋亡率明显增加,与对照组比较差异有显著意义(8.02% vs 4.38%,P＜0.01;11.05% vs 4.35%,P＜0.01;24.86% vs 4.54%,P＜0.01),与单用缬草波春组比较差异无显著意义.缬草波春降低MKN-45胃癌细胞株Survivin mRNA的表达,并有浓度依赖性和时间依赖性,而且使MKN-45胃癌细胞株P53蛋白表达增加,Survivin蛋白表达降低,均有浓度依赖性.结论:缬草波春可诱导MKN-45细胞凋亡,其作用可部分被Caspase-3,Caspase-9抑制剂所抑制,但不能被Caspase-8抑制剂所抑制.缬草波春诱导MKN-45胃癌细胞株凋亡与P53蛋白表达提高及Survivin mRNA和Survivin蛋白低表达降低有关.     

感染后肠易激综合征与溃疡性结肠炎缓解期患者肠黏膜细胞因子表达的相关性

目的:探讨感染后肠易激综合征(PI-IBS)与溃疡性结肠炎(UC)缓解期患者结肠黏膜细胞因子表达的相关性.方法:PI-IBS组26例,UC组45例及对照组30例,结肠镜下活检降结肠和直肠黏膜标本,采用免疫组化SABC法检测其肠黏膜P物质(SP)与IL-2,IFN-γ的表达情况.结果:PI-IBS组降结肠和直肠黏膜IFN-γ和IL-2阳性率表达、SP强度均值和面积高于对照组(IFN-γ:χ2=13.781,14.012,P＜0.01;IL-2:χ2=13.890,13.931,P＜0.01;SP强度:t=3.623,3.722,P＜0.01;SP面积:t=3.454,3.561,P＜0.01),但与UC组患者无显著差异.降结肠、直肠黏膜IFN-γ,IL-2阳性表达的PI-IBS患者,SP强度均值(t=2.202,2.220,P＜0.05)、面积高于对照组(t=2.301,2.252,P＜0.05),与UC组患者也无显著差异.结论:PI-IBS和UC缓解期患者细胞因子表达无显著差异.从神经-免疫机制上分析认为IBS与炎症性肠病(IBD)之间存在某种相关性,IBS可能是轻微的IBD.     

缬草波春联合Caspases抑制剂诱导MKN45胃癌细胞凋亡

目的 研究中草药缬草提取物缬草波春联合Caspases抑制剂诱导MKN45胃癌细胞凋亡的作用。方法 将MKN45胃癌细胞分成4组:第1组加入同体积的生理盐水为对照;第2组分别加入浓度为10μM的Caspases-3、-8、-9抑制剂;第3组加入浓度为100 mg／L的缬草波春;第4组加入浓度为10 μM的Caspases-3、-8、-9抑制剂+浓度为100 mg／L的缬草波春混合物。药物作用24小时、48小时、72小时后,用流式细胞计分别检测凋亡率。结果　24、48、72小时作用后,第2组诱导MKN45细胞的凋亡率与对照组相似(P>0.05);第3组诱导MKN45细胞的凋亡率明显高于照组相(P<0.01);第4组中缬革波春联合Caspases-3、-9抑制剂诱导MKN45细胞的凋亡率均与对照组相似(P>0.05);缬草波存与Caspases-8抑制剂联合应用组诱导MKN45细胞的凋亡率明显高于对照组比(P<0.01),与第2组相似(P>0.05)。结论 缬草波春能诱导MKN45胃癌细胞凋亡,诱导凋亡能被Caspases-3、-9抑制剂抑制,Casoases-8抑制剂对缬草波春诱导的调亡无影响。     

老年慢性功能性便秘患者结肠和肛管直肠动力学的改变

目的 探讨功能性便秘患者结肠和肛管直肠动力学改变及其对便秘分型、临床治疗的指导意义.方法 对我院42例老年功能性便秘患者(CFC)及20例健康对照者,采用不透X线标记物法测定结肠通过时间(CTT),同时应用8通道水灌注式下消化道压力检测系统进行直肠、肛管动力学测定.结果 (1)老年CFC组全结肠通过时间及乙状结肠通过时间分别为(49.0±16.4)h和(20.1±13.5)h,较对照组(25.2±7.7)h和(7.8±4.1)h明显延长(t=6.16和t=3.97,均P<0.05);(2)老年CFC患者模拟排便时肛管压力为(39.6±15.7)mmHg,对照组为(17.6±9.3)mmHg,两组比较差异有统计学意义(t=5.79,P<0.05),老年CFC组13例患者模拟排便时出现肛管压力反常升高;老年CFC组直肠初始感觉阈和最大耐受容量分别为(49.2±10.5)ml和(175.2±52.6)ml,高于对照组的(33.6±8.5)ml和(123.4±39.1)ml,差异均有统计学意义(t=5.79和t=3.91,均P<0.05);直肠肛门抑制反射松弛率两组分别为59.5%和85.0%(x2=4.03,P相似文献   

内脏高敏感大鼠结肠5-羟色胺转运体蛋白的表达

目的:探讨5-羟色胺转运体蛋白(SERT)在内脏高敏感性中的作用,为功能性胃肠病的发病机制研究提供理论基础.方法:采用乳鼠醋酸灌肠建立大鼠慢性内脏高敏感动物模型,同时设立对照组.待乳鼠成年后应用直肠内球囊扩张评估腹壁撤离反射(AWR)的方法,评估其内脏敏感性;检测髓过氧化物酶(MPO)评价其肠道黏膜炎症程度;用RT-PCR方法评价大鼠结肠SERT的mRNA水平,免疫组织化学方法评价大鼠结肠SERT的表达:用ELISA方法检测血浆和结肠组织5-HT水平.结果:乳鼠醋酸灌肠建立的大鼠慢性内脏高敏感模型组与对照组相比HE染色显示结肠黏膜未见明显急、慢性炎症改变;两组大鼠结肠组织MPO水平没有显著性差异;在不同容量下的AWR评分慢性内脏高敏感模型组显著高于对照组(P<0.01).血浆5-HT水平慢性内脏高敏感模型组明显高于对照组(95.75±15.99vs 72.17±8.01,P<0.01),而两组结肠组织5-HT含量没有明显差异.免疫组织化学研究显示内脏高敏感模型组结肠上皮SERT表达水平显著低于对照组(0.187±0.010 vs 0.191±0.011,P<0.011,而其结肠SERT mRNA水平显著高于对照组(16.02±3.7 vs 10.05±2.12,P<0.01).结论:内脏高敏感大鼠外周5-HT水平的增高主要来源于其灭活的减少而非合成的增加,与SERT的关系密切.结肠SERT可能具有不同的亚型和功能.     

感染后与非感染后IBS患者结肠黏膜SP与IL-2、IFN-γ表达的相关性

目的:探讨肠道感染对IBS患者结肠黏膜SP,IL-2,IFN-γ表达的影响.方法:77例IBS患者(PI-IBS组26例,非PI-IBS组51例)及30例对照者,结肠镜下活检降结肠和直肠黏膜标本,采用免疫组化检测其肠黏膜SP与IL-2,IFN-γ的表达情况.结果:PI-IBS患者结肠黏膜SP的表达高于非PI-IBS患者(t=2.321,2.452,2.414,2.520,P<0.05)和对照组(t=3.623,3.722,3.454,3.561,P<0.01);PI-IBS患者结肠黏膜IFN-γ和IL-2阳性率表达高于非PI-IBS患者(χ2=10.010,9.892,9.984,10.152,P<0.05)和对照组(χ2=13.781,13.890,14.012,13.931,P<0.01);IFN-γ和IL-2阳性表达的PI-IBS患者结肠黏膜SP表达高于非PI-IBS患者(t=2.182,2.230,2.194,2.174,P<0.05)和对照组(t=2.202,2.220,2.301,2.252,P<0.05).非PI-IBS患者结肠黏膜IFN-γ和IL-2阳性SP的表达者与对照组比较无明显差异.结论:感染可能通过肠黏膜神经-免疫/炎症系统的改变参与了IBS的发病.     

夏枯草胶囊对溃汤性结肠炎大鼠外周血T淋巴细胞亚群表达的影响

目的:观察夏枯草胶囊对大鼠溃疡性结肠炎(UC)外周血T淋巴细胞亚群的影响.方法:采用异种异体结肠粘膜组织致敏法.将SD大鼠随机分为空白对照组,模型对照组,夏枯草胶囊高、中、低剂量组,柳氮磺胺吡啶组.连续给药4周.空白对照组和模型对照组灌胃给予0.85%氯化钠溶液10 ml/kg;末次给药后24 h,大鼠眼眶采血,测定外周血T淋巴细胞亚群;处死大鼠,计数全结肠溃疡点和充血点;称结肠湿重;计算肠重指数.结果:夏枯草胶囊3个剂量组大鼠:能显著降低或减少溃疡数和充血指数(P<0.01);结肠重量和肠重指数有所增加,其中高剂量组与模型对照组比较差异有统计学意义(P<0.01);均能上调T淋巴细胞亚群值,以高剂量组显著(P<0.05).结论:夏枯草胶囊可能是通过调节外周血T淋巴细胞亚群的作用,显示其清热解毒散结,调节免疫的作用,这可能是治疗UC的作用机制之一.     

4-氨基水杨酸对大鼠实验性结肠炎中性粒细胞趋化、活化及凋亡的影响

目的 观察4-氨基水杨酸(4-ASA)对三硝基苯磺酸(TNBS)诱导的大鼠实验性结肠炎炎症损伤、肠组织一氧化氮合酶(iNOS)表达、血中性粒细胞(PMN)凋亡及血清白细胞介素(IL)-8水平等的影响,探讨4-ASA对炎症性肠病(IBD)的治疗作用及机制.方法 40只SD大鼠分为正常对照组(n=10)和实验组(n=30),实验组建立大鼠结肠炎模型.建模第5天将实验组按照处理方式分为实验对照组(n=10,0.9%氯化钠1 ml灌肠),5-ASA组[n=10,5-ASA液(200 mg/kg)1 ml灌肠]和4-ASA组[n=10,4-ASA液(200 mg/kg)1 ml灌肠].连续治疗7 d后处死动物,取病变段肠组织,行结肠大体损伤及结肠组织学损伤评分;生化法检测髓过氧化物酶活性;免疫组化法检测肠组织iNOS表达量;流式细胞术检测血PMN凋亡率;酶联免疫吸附法检测血清IL-8浓度.结果 经4-ASA治疗7d后,4-ASA组大鼠体重明显较实验对照组增加(P<0.01,t=14.09);疾病活动指数评分、大体评分、组织学评分和MPO活性显著较实验对照组降低(t值分别=7.87、18.37、6.66和19.60,P值均<0.01).而5-ASA组与4-ASA组间上述各指标差异均无统计学意义(P值均>0.05).实验对照组肠组织iNOS表达率为(73.55±5.15)%,较正常对照组显著增加[(5.95±1.45)%,t=39.93,P<0.01)];5-ASA和4-AsA组大鼠肠组织iNOS表达率分别为(37.80±3.82)%和(42.27±3.52)%,均较实验对照组显著降低(t值分别=17.62和15.76,P值均<0.01).实验对照组血清IL-8的平均浓度明显高于正常对照组(t=25.25,P<0.01);5-ASA和4-ASA组明显低于实验对照组(t值分别=12.31和11.57,P值均<0.01).实验对照组血PMN凋亡率明显低于正常对照组(t=11.48,P<0.01);5-ASA和4-ASA组凋亡率明显高于实验对照组(t值分别=7.51和10.47,P值均<0.01).结论 4-ASA灌肠对实验性结肠炎大鼠具有显著的治疗作用,其治疗机制可能与降低PMN的趋化与激活、上调血PMN凋亡率、减少肠组织局部损伤因子有关.     

Cisapride accelerates colonic transit in constipated patients with colonic inertia

A double-blind cross-over trial of oral cisapride 10 mg before meals and placebo was performed to determine its effects on colonic transit in patients with severe idiopathic constipation. Nine patients with less than 3 spontaneous bowel movements/wk were studied. After passing a tube to the cecum, 50 muCi of 111In-DTPA were instilled into the cecum and followed for 48 h using colonic transit scintigraphy. In the group as a whole, cisapride had little effect on transit. The patients were then divided into two groups based on transit: functional rectosigmoid obstruction (FRSO) and colonic inertia (CI). In the CI group, cisapride accelerated the half emptying time of the cecum and ascending colon from 2.50 to 1.21 h (p less than 0.05). The progression of the geometric center was also faster after cisapride in CI. In FRSO, the geometric center was unchanged by cisapride except at 48 h. Cisapride thus has a prokinetic effect on colonic transit in patients with severe idiopathic constipation, colonic inertia subtype. It may be a useful agent in the treatment of this group of patients.     

Bleeding colonic diverticula

Diverticula of the large intestine constitute a common source of lower gastrointestinal (GI) bleeding both occult and massive and are a particular common cause of right-sided colonic hemorrhage. Bleeding in all cases is due to rupture of the underlying vasa rectum. In all cases, rupture of the artery is not circumferential, but eccentric having occurred toward the lumen of the diverticula. It is rare to see either acute or chronic diverticulitis associated with this situation. Lower GI bleeding is frequent in the elderly secondary to diverticular disease and occurs in about 10% to 30% GI bleeds and actually is much less frequent than upper GI bleeding. Diverticular disease actually is uncommon in people under the age of 40. However, by the age of 50 almost one-third of the population has diverticulosis. Ninety percent of the diverticula are in the left colon, but bleeding is from the right colon at least 50% of the time. Diverticular hemorrhage will cease spontaneously in about 90% cases. Most often, there is no inflammatory process around the diverticular bleeding. Hypertension even may be a predisposing factor. Also anticoagulation, diabetes mellitus, and ischemic heart disease are associated with diverticular hemorrhage. As far as treatment is concerned, conservative therapy is usually the best approach. One would like to avoid angiography and surgery if at all possible. There is a significant recurrence of bleeding in those patients who are treated even with angiography and with surgery. Etiology of the bleeding is not really well understood and the diagnosis and treatment is quite difficult in some situations.     

Giant colonic diverticulum

PURPOSE: Giant colonic diverticulum are rare, with 103 reported cases in 95 patients. The experience of any one surgeon is limited. We aimed to retrospectively review our experience and to review the literature on origin, pathology, and management of this rare and unusual problem. METHOD: Cases were identified by review of pathologic database and by computerized audit from three hospitals. RESULTS: Five giant colonic diverticulum were identified in four patients, and the pathology and management were reviewed. CONCLUSION: A definition and classification system of giant colonic diverticulum is suggested. Giant colonic diverticulum should be the universal term to cover all colonic diverticulum larger than 4 cm, and we suggest that there are two types based on histology. Literature review reveals 103 reported cases in 95 patients. Type I (87 percent) is a pseudodiverticulum, perhaps related to conventional diverticular disease, whereas Type II (13 percent) is a true diverticulum, which is probably a type of communicating cystic congenital duplication. These lesions tend to occur in the sigmoid colon (93 percent) and present with complications similar to conventional diverticular disease. In the presence of conventional diverticular disease, consideration should be given to anterior resection, and in the absence, diverticulectomy should be considered.