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91.
探讨术苓健脾胶囊(术苓)对2,4,6-三硝基苯磺酸(TNBS)诱导的大鼠实验性结肠炎的作用及其机制。采用2.5%TNBS灌肠制备大鼠实验性结肠炎模型。将大鼠随机分为正常组、模型组、肠炎宁(180 mg/kg)组以及术苓低剂量(40 mg/kg)、高剂量(120 mg/kg)组。造模后药物治疗7 d后处死大鼠。其间每日记录大鼠体重,观察大鼠疾病活动状态。实验结束后,取结肠组织进行HE病理学分析、检测结肠组织中髓过氧化物酶(MPO)酶活、诱导型一氧化氮合酶(iNOS)、炎性细胞因子(IL-6、IL-1β、IFN-γ、IL-10)及紧密连接蛋白(occludin、ZO-1)的表达水平,并检测血清中炎性细胞因子(IL-6、IL-1β)的含量。结果表明,与模型组相比,术苓给药显著缓解了TNBS造模引起的体重下降、疾病活动指数(DAI)升高,缓解了结肠组织的缩短、水肿以及病理学损伤,减少了炎性细胞浸润、隐窝的破坏与杯状细胞的丢失,降低了结肠组织MPO酶活性、iNOS与炎性细胞因子的水平,增加了结肠紧密连接蛋白的表达,同时降低了血清中的炎性因子的含量。结果表明,术苓通过降低炎性因子水平,增加肠道紧密...  相似文献   
92.
5-氨基水杨酸灌肠对大鼠免疫性结肠炎的影响   总被引:5,自引:0,他引:5  
目的 探讨5-氨基水杨酸(5-ASA)灌肠对大鼠三硝基苯磺酸(TNBS)诱导的结肠炎的作用.方法用TNBS诱发大鼠结肠炎.造模7天后,用不同剂量的5-ASA(25、50、100mg·kg-1·d-1)开始灌肠.观察大鼠粪隐血(OB)反应强度、结肠大体形态和组织学改变,并检测肠黏膜髓过氧化物酶(MPO)活性.结果 5-ASA灌肠可明显降低结肠黏膜损伤指数(CMDI)、OB反应强度、MPO活性及组织学评分(HS),各剂量组间有一定的量效关系.结论 5-ASA灌肠对TNBS诱导的大鼠结肠炎有保护作用,且与剂量有一定关系.  相似文献   
93.
结肠康治疗慢性非特异性溃疡性结肠炎的实验研究   总被引:13,自引:0,他引:13  
根据献方法,制作慢性非特异性溃疡性结肠炎的动物模型。观察结肠康、柳氮磺胺吡啶(SASP)治疗实验动物的慢性非特异性溃疡性结肠炎(CNUC)前后的变化,并作统计学处理。结果表:结肠康治疗后模型动物的Ea-RFC(活性E-玫瑰花环成率)、Et-FRC(总E-玫瑰花环形成率)、LTR)淋巴转化率)显升高(P〈0.05或P〈0.01),IgG降低;SASP治疗后模动物Ea-RFC、Et-FRC、LTR  相似文献   
94.
Primary and recurrent cytomegalovirus (CMV) infections frequently cause CMV colitis in immunocompromised as well as inflammatory bowel disease (IBD) patients. Additionally, colitis occasionally occurs upon primary CMV infection in patients who are apparently immunocompetent. In both cases, the underlying pathophysiologic mechanisms are largely elusive - in part due to the lack of adequate access to specimens. We employed the mouse cytomegalovirus (MCMV) model to assess the association between CMV and colitis. During acute primary MCMV infection of immunocompetent mice, the gut microbial composition was affected as manifested by an altered ratio of the Firmicutes to Bacteroidetes phyla. Interestingly, these microbial changes coincided with high-titer MCMV replication in the colon, crypt hyperplasia, increased colonic pro-inflammatory cytokine levels, and a transient increase in the expression of the antimicrobial protein Regenerating islet-derived protein 3 gamma (Reg3γ). Further analyses revealed that murine and human intestinal epithelial cell lines, as well as primary intestinal crypt cells and organoids represent direct targets of CMV infection causing increased cell death. Accordingly, in vivo MCMV infection disrupted the intestinal epithelial barrier and increased apoptosis of intestinal epithelial cells. In summary, our data show that CMV transiently induces colitis in immunocompetent hosts by altering the intestinal homeostasis.  相似文献   
95.
《Immunobiology》2023,228(4):152386
Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon that can be influenced by microRNAs (miRNAs). This study aims to investigate the impact of miR-146a-5p on lipopolysaccharide (LPS)-induced Caco-2/HT-29 cell autophagy and NLRP3 inflammasome activation and the underlying mechanism, with the aim of identifying potential therapeutic targets. We used LPS to establish Caco-2/HT-29 cell models and measured cell viability by CCK-8. The levels of miR-146a-5p, RNF8, markers of NLRP3 inflammasome activation and autophagy, proteins involved in the Notch1/mTORC1 pathway, and inflammatory factors were assessed by RT-qPCR, Western blot, and ELISA. Intestinal epithelial barrier function was evaluated by measuring transepithelial electrical resistance. Autophagic flux was measured using tandem fluorescent-labeled LC3. miR-146a-5p was highly-expressed in LPS-induced Caco-2/HT-29 cells, and autophagy flux was blocked at the autolysosomal stage after LPS induction. Inhibition of miR-146a-5p suppressed NLRP3 inflammasome activation, reduced intestinal epithelial barrier damage, and facilitated autophagy inhibition in LPS-induced Caco-2/HT-29 cells. The autophagy inhibitor NH4Cl partially nullified the inhibitory effects of miR-146a-5p inhibition on NLRP3 inflammation activation. miR-146a-5p targeted RNF8, and silencing RNF8 partly abrogated the action of miR-146a-5p inhibition on promoting autophagy and inhibiting NLRP3 inflammasome activation. miR-146a-5p inhibition suppressed the Notch1/mTORC1 pathway activation by upregulating RNF8. Inhibition of the Notch1/mTORC1 pathway partially nullified the function of silencing RNF8 on inhibiting autophagy and bolstering NLRP3 inflammasome activation. In conclusion, miR-146a-5p inhibition may be a potential therapeutic approach for UC, as it facilitates autophagy of LPS-stimulated Caco-2/HT-29 cells, inhibits NLRP3 inflammasome activation, and reduces intestinal epithelial barrier damage by upregulating RNF8 and suppressing the Notch1/mTORC1 pathway.  相似文献   
96.
Although excessive immune responses by Th17 cells, a helper T cell subset, are implicated in the pathogenesis of inflammatory bowel disease (IBD), the mechanism by which its localization in an inflamed colon is regulated remains unclear. Chemokines and their receptors are involved in the pathogenesis of IBD, however, the relative significance of each receptor on Th17 cells remains unknown. We generated C–C motif chemokine receptor 2 (CCR2) knockout (KO) and CCR6 KO mice in the syngeneic background using the CRISPR/Cas9 system and found that the phenotypes of experimental colitis worsened in both mutant mice. Surprisingly, the phenotype of colitis in CCR2/CCR6-double knockout (CCR2/6 DKO) mice was opposite to that of the single-deficient mice, with significantly milder experimental colitis (p < .05). The same was true for the symptoms in CCR6 KO mice, but not in wild type mice treated with a CCR2 inhibitor, propagermanium. Colonic CCR2+CCR6+ Th17 cells produced a potentially pathogenic cytokine GM-CSF whose levels in the gut were significantly reduced in CCR2/6 DKO mice (p < .05). These results suggest that GM-CSF-producing CCR2+CCR6+ Th17 cells are pathogenic and are attracted to the inflamed colon by either CCR2 or CCR6 gradient, which subsequently exacerbates experimental colitis in mice.  相似文献   
97.
目的研究溃疡性结肠炎患者的炎性因子水平、肠道菌群分布及发病相关危险因素,为溃疡性结肠炎的防治工作提供科学依据。方法以2020年6月至2021年5月在文昌市某医院就诊的溃疡性结肠炎患者作为病例组,同时选取(按年龄相差0.5岁,性别相同招揽志愿者参与本研究)同期在该医院进行健康体检者作为对照组。所有研究对象进行问卷调查、肠道菌群检测及炎症因子检测,采用描述性分析方法对2组相关指标进行比较,并对溃疡性结肠炎发病影响因素进行单、多因素分析。结果共纳入溃疡性结肠炎病例(病例组)和健康体检者(对照组)各200例,男性各99例,女性各101例,病例组平均年龄(43.17±8.72)岁,对照组平均年龄(43.54±9.11)岁,2组的年龄、性别分布差异均无统计学意义(均P>0.05)。病例组主要检出的双歧杆菌、乳杆菌数量低于对照组,拟杆菌、肠杆菌、肠球菌、梭杆菌数量高于对照组(均P<0.01)。病例组除白细胞介素(IL)-4水平低于对照组,IL-6、IL-17、IL-23以及肿瘤坏死因子-α(TNF-α)均高于对照组(均P<0.01)。饮酒(OR=3.526)、吸烟(OR=1.272)、饮食不洁(OR=4.592)、存在合并感染(OR=2.146)、情绪紧张(OR=3.919)均为溃疡性结肠炎发病的危险因素。结论溃疡性结肠炎患者肠道菌群种类、数量分布不平衡,血清炎症因子水平明显上升。良好的生活行为习惯以及积极地健康教育可降低溃疡性结肠炎的发生风险。  相似文献   
98.
PURPOSE: Acute pouchitis is a troublesome complication after restorative proctocolectomy. Deficiency of fuel, especially short chain fatty acids (SCFA), produced by anaerobic bacterial fermentation of saccharides, is implicated in ulcerative and diversion colitis. Our hypothesis was that SCFA deficiency occurs in acute pouchitis, and correction of the deficiency is associated with resolution of pouchitis. METHODS: Thirty-two patients were studied, 10 with histologically confirmed acute pouchitis and 22 with healthy pouches. Stool concentrations of SCFA (acetic, propionic, butyric, and valeric acids) were determined by gas-liquid chromatography. Quantitative bacteriologic studies of stool were carried out, and four-quadrant pouch biopsies were assessed by a pathologist who was unaware of the clinical state. Patients with pouchitis were treated for six weeks with metronidazole and given dietary advice to increase their intake of fermentable saccharides. RESULTS: Stool concentrations of SCFA were significantly less in pouchitis patients compared with patients with healthy pouches (340 mol/g (range, 124–492) vs.93 (range, 44–136) P<0.01). No differences in anaerobic or aerobic counts were seen. Resolution of pouchitis was associated with a significant increase in SCFA, but anaerobic counts fell. CONCLUSION: Deficiency of SCFA is implicated in acute pouchitis Read at the meeting of The American Society of Colon and Rectal Surgeons, Orlando, Florida, May 8 to 13, 1994.  相似文献   
99.
(Received for publication on Sept. 21, 1998; accepted on May 27, 1999)  相似文献   
100.
Patients with primary sclerosing cholangitis (PSC) in Japan have two peaks in age distribution, one in their twenties and the other in their fifties and sixties. PSC patients in Japan have different characteristics from those in other countries: there is a higher incidence of eosinophilia (27%) and positivity for anti-nuclear antibody (30%), less frequent complication with inflammatory bowel diseases (IBD; 21%), and more frequent complication with chronic pancreatitis (15%). In younger patients in Japan (those aged less than 40 years), the incidence of positivity for anti-nuclear antibody was lower (20% vs 38% P < 0.05), complication with IBD was more frequent (39% vs 9% P < 0.01), complication with chronic pancreatitis was less frequent (4% vs 22% P < 0.01), and damage to both the intra- and extrahepatic bile ducts was more frequent (89% vs 56% P < 0.01) than in older patients (those aged 40 years or more). These findings suggest that younger PSC patients in Japan have characteristics similar to those of patients in other countries, and that in Japan older PSC patients have a different pathogenesis from that of younger patients. Received for publication on Feb. 16, 1999; accepted on April 5, 1999  相似文献   
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