您的位置：山东大学 -> 科技期刊社 -> 《山东大学学报（医学版）》

山东大学学报（医学版） ›› 2016, Vol. 54 ›› Issue (12): 58-61.doi: 10.6040/j.issn.1671-7554.0.2016.464

• 临床医学 • 上一篇    下一篇

血管内皮细胞活化在感染后肠易激综合征发病机制中的作用

李倩1,戴桃李1,韩炜1,郭成浩2   

  1. 1.山东大学齐鲁医院消化内科, 山东 济南 250012;2.山东大学医学院病理教研室, 山东 济南 250012
  • 收稿日期:2016-04-25 出版日期:2016-12-10 发布日期:2016-12-10
  • 通讯作者: 郭成浩. E-mail:chenghaoguo@sdu.edu.cn E-mail:chenghaoguo@sdu.edu.cn
  • 基金资助:
    国家自然科学基金(30700358)

Role of vascular endothelial cell activation in the pathogenesis of post infectious irritable bowel syndrome

LI Qian1, DAI Taoli1, HAN Wei1, GUO Chenghao2   

  1. 1. Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    2. Department of Pathology, Medical School of Shandong University, Jinan 250012, Shandong, China
  • Received:2016-04-25 Online:2016-12-10 Published:2016-12-10

PDF (PC)

150

摘要： 目的 研究感染后肠易激综合征(PI-IBS)患者中肠血管内皮细胞形态以及血浆中内皮素(ET)和一氧化氮(NO)表达水平的变化,明确血管内皮细胞活化在PI-IBS发病机制中的作用。 方法 同期收集就诊的PI-IBS患者28例和正常对照组12例,采集所有研究对象的空腹血标本和结肠标本。用光学显微镜观察内皮细胞形态和变化,用放射免疫法和硝酸还原法分别检测血浆中ET和NO表达水平的变化。 结果 PI-IBS患者内皮细胞形态较正常对照组发生显著变化,功能上的变化表现为血浆中ET(55.49±13.49)ng/L和NO(75.90±16.52)μmol/L表达水平较正常对照组［(43.40±13.69)ng/L和(62.48±15.63)μmol/L］明显增高(P<0.05)。 结论 血管内皮细胞活化与PI-IBS的发病机制可能密切相关。

关键词: 内皮素, 一氧化氮, 内皮细胞活化, 形态学, 感染后肠易激综合征

Abstract: Objective To investigate the morphological changes of vascular endothelial cells as well as changes in the level of plasma endothelin(ET)and nitric oxide(NO)in patients with post infectious irritable bowel syndrome(PI-IBS), in order to clarify the possible role of vascular endothelial cell activation in the pathogenesis of PI-IBS. Methods The mucosa biopsy samples and plasma were obtained from 28 PI-IBS patients and 12 healthy controls during the same period. The morphological changes of vascular endothelial cells were observed with light microscope. The plasma ET and NO levels in both groups were measured with radioimmunoassay and nitrate reductase method. Results There were more significant morphological changes in vascular endothelial cells in the PI-IBS patients than in the controls. The plasma ET and NO levels of the PI-IBS patients were(55.49±13.49)ng/L and(75.90±16.52)μmol/L, respectively, which were significantly higher than those of the controls［(43.40±13.69)ng/L and(62.48±15.63)μmol/L, both P<0.05］. Conclusion The vascular endothelial cell activation may be closely related to the pathogenesis of PI-IBS.

Key words: Vascular endothelial cell activation, Endothelin, Nitric oxide, Post infectious irritable bowel syndrome, Morphology

中图分类号: 

  • R574
[1] Serghini M, Karoui S, Boubaker J, et al. Post-infectious irritable bowel syndrome[J]. Tunis Med, 2012, 90(3): 205-213.
[2] Spiller RC, Jenkins D, Thornley JP, et al. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome[J]. Gut, 2000, 47(6): 804-811.
[3] Sundin J, Rangel I, Kumawat AK, et al. Aberrant mucosal lymphocyte number and subsets in the colon of post-infectious IBS patients[J]. Scand J Gastroenterol, 2014, 49(9): 1068-1075.
[4] Cotton JA, Beatty JK, Buret AG. Host parasite interactions and pathophysiology in Giardia infections[J]. Int J Parasitol, 2011, 41(9): 925-933.
[5] Martínez C, González-Castro A, Vicario M, et al. Cellular and molecular basis of intestinal barrier dysfunction in the irritable bowel syndrome[J]. Gut Liver, 2012, 6(3): 305-315.
[6] Zhou Q, Zhang B, Verne GN. Intestinal membrane permeability and hypersensitivity in the irritable bowel syndrome[J]. Pain, 2009, 146(1-2): 41-46.
[7] Kwok W, Clemens MG. Rho-kinase activation contributes to Lps-induced impairment of endothelial nitric oxide synthase activation by endothelin-1 in cultured hepatic sinusoidal endothelial cells[J]. Shock, 2014, 42(6): 554-561.
[8] Kim YJ, Koo TY, Yang WS, et al. Activation of spleen tyrosine kinase is required for TNF-α-induced endothelin-1 upregulation in human aortic endothelial cells[J]. FEBS Lett, 2012, 586(6): 818-826.
[9] Zhang J, Defelice AF, Hanig JP, et al. Biomarkers of endothelial cell activation serve as potential surrogate markers for drug-induced vascular injury[J]. Toxicol Pathol, 2010, 38(6): 856-871.
[10] Dai C, Guandalini S, Zhao DH, et al. Antinociceptive effect of VSL#3 on visceral hypersensitivity in a rat model of irritable bowel syndrome: a possible action through nitric oxide pathway and enhance barrier function[J]. Mol Cell Biochem, 2012, 362(1-2): 43-53.
[11] Rapoport RM. Acute nitric oxide synthase inhibition and endothelin-1-dependent arterial pressure elevation[J]. Front Pharmacol, 2014, 5: 57. doi: 10.3389/fphar.2014.00057.
[12] Saini V, Bhatnagar MK, Bhattacharjee J. Association of endothelial dysfunction with endothelin, nitric oxide and eNOS Glu298Asp gene polymorphism in coronary artery disease[J]. Dis Markers, 2011, 31(4): 215-222.
[13] 陈忠龙, 吴小南. 肠黏膜屏障与胃肠疾病[J]. 海峡预防医学杂志, 2007, 13(2): 31-33.
[14] Dunlop SP, Hebden J, Campbell E, et al. Abnormal intestinal permeability in subgroups of diarrhea-predominant irritable bowel syndromes[J]. Am J Gastroenterol,2006, 101(6): 1288-1294.
[15] Vivinus-Nébot M, Dainese R, Anty R, et al. Combination of allergic factors can worsen diarrheic irritable bowel syndrome: role of barrier defects and mast cells[J]. Am J Gastroenterol 2012, 107(1): 75-81.
[16] Wang H, Gong J, Wang W, et al. Are there any different effects of Bifidobacterium, Lactobacillus and Streptococcus on intestinal sensation, barrier function and intestinal immunity in PI-IBS mouse model?[J]. PLoS One, 2014, 9(3): e90153. doi: 10.1371/journal.pone.0090153.
[17] Halliez MC, Motta JP, Feener TD, et al. Giardia duodenalis induces paracellular bacterial translocation and causes postinfectious visceral hypersensitivity[J]. Am J Physiol Gastrointest Liver Physiol, 2016, 310(8): G574-585.
[1] 刘琳,刘春红,王得翔,吴金香,赵继萍,刘甜,张元元,王俊飞,柳亚慧,曹柳兆,董亮. 应用呼出气一氧化氮联合脉冲振荡肺功能评估哮喘患者的小气道功能[J]. 山东大学学报（医学版）, 2016, 54(8): 78-83.
[2] 李欣,王公明,王红,王岩,张立功,张乐,刘蓓,张孟元. 诱导型一氧化氮合成酶参与大鼠心脏缺血后处理延迟相的保护作用[J]. 山东大学学报（医学版）, 2016, 54(2): 16-20.
[3] 潘艳艳,孙永超,赵翠芬,孔清玉. 波生坦治疗婴儿先心病合并肺动脉高压的临床观察[J]. 山东大学学报（医学版）, 2016, 54(2): 53-56.
[4] 刘慧敏, 刘邓, 李晓宇, 邹淑奉, 姜黎民, 李玉环. 半边莲生物碱对肺动脉高压大鼠ET-1信号通路的影响[J]. 山东大学学报（医学版）, 2015, 53(8): 1-4.
[5] 刘杰, 刘金之, 林艳, 黄占, 王爱华. 超时间窗溶栓治疗对大鼠急性脑梗死后自由基活性和Caspase-3表达的影响[J]. 山东大学学报（医学版）, 2015, 53(4): 26-30.
[6] 刘斌钰, 刘斌焰, 邢雁霞, 何引飞, 徐欣. PRP在颅骨缺损修复中血管化的实验研究[J]. 山东大学学报（医学版）, 2015, 53(2): 27-33.
[7] Gleniece Irving, 王硕, 王辉, 郭盈, 姜路路, 赵秀兰, 谢克勤. 二硫化碳暴露对大鼠学习能力的影响[J]. 山东大学学报（医学版）, 2015, 53(10): 82-86.
[8] 李恒渠, 王登海. 外周血液涂片镜检在血常规检查中作用[J]. 山东大学学报（医学版）, 2014, 52(S2): 27-28.
[9] 吴宏图, 丁娴, 张磊, 曹兴丽, 王峥艳, 单春明, 刘平. 儿童咳嗽变异性哮喘FeNO、hs-CRP及 IgE水平变化及意义[J]. 山东大学学报（医学版）, 2014, 52(S2): 82-83.
[10] 付庆元, 戴桂强, 张松, 安洪春, 梁世民. 西洋参茎叶皂苷对脑梗死大鼠ET-1、VEGF及脑梗死面积的影响[J]. 山东大学学报（医学版）, 2014, 52(9): 30-33.
[11] 程龙凤1，潘燕1，刘尚明2，王立言2，张岫美3，徐红岩4，李红宇5. 脑淋巴液滞留对大鼠前额叶皮质区诱导型一氧化氮合成酶表达量的影响及羟基红花黄素A对神经元的保护作用[J]. 山东大学学报（医学版）, 2014, 52(6): 7-11.
[12] 王旭阳, 江敦清, 陈世文, 田恒力, 刘芬, 李志强. 封闭内源性NT-3在脊髓损伤后期神经元有髓神经纤维出芽中的作用[J]. 山东大学学报（医学版）, 2014, 52(12): 5-9.
[13] 刘婧源，张晓，安婕. 不同冲洗剂处理对纤维桩剪切粘接强度的影响[J]. 山东大学学报(医学版), 2013, 51(4): 30-33.
[14] 张艳祥1,2,迟兆富1,刘学伍1,杨雪1,程蕊1. 海马内注射脂多糖导致痫性发作及其机制[J]. 山东大学学报(医学版), 2012, 50(9): 1-5.
[15] 陈伟，谈红，李晓燕，杨燕，韦修莹，陈英剑，张红明. 冠心病患者外周血内皮祖细胞数量差异及其对内皮功能的影响[J]. 山东大学学报(医学版), 2012, 50(8): 73-76.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
版权所有 © 2018 《山东大学学报(医学版)》编辑部　
地址:山东大学科技期刊社（济南市历城区山大南路27号山东大学中心校区明德楼B座721室） 电话: 0531-88366918 E-mail: xbyxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发