穴位埋线治疗实验性结肠炎大鼠的机制探讨

被引:2
作者
张夏毅
沈霖
范恒
梁丽
廖弈
机构
[1] 华中科技大学同济医学院附属协和医院中西医结合科
关键词
结肠炎; 穴位埋线; NF-κBp65; STAT6;
D O I
暂无
中图分类号
R245 [针灸学、针灸疗法];
学科分类号
100512 ;
摘要
目的:检测TNBS诱导实验性结肠炎大鼠在穴位埋线治疗前后的NF-κBp65和STAT6mRNA的表达水平,初步阐明穴位埋线治疗实验性结肠炎大鼠的作用机理。方法:18只雄性大鼠随机分为正常组、模型组、穴位埋线组,每组6只。除正常对照组未行造模外,其余2组大鼠均采用TNBS造模。模型组不设干预,正常饮食;穴位埋线组进行穴位埋线治疗。治疗15d后观察大鼠的结肠病理组织学改变,用western blot法检测大鼠脾淋巴细胞NF-κBp65蛋白的表达;用RT-PCR法检测大鼠结肠组织STAT6mRNA的表达。结果:穴位埋线组的大鼠腹泻、黏液脓血便症状得到较快改善,大鼠黏膜组织损伤也明显改善。与正常组相比,模型组大鼠NF-κBp65和STAT6mRNA增多(P<0.01);与模型组比较,穴位埋线组NF-κBp65和STAT6mRNA减少(P<0.01)。结论:穴位埋线能通过NF-κB和STAT6双信号途径下调炎症因子,从而发挥治疗作用。
引用
收藏
页码:527 / 529
页数:3
相关论文
共 9 条
[1]  
Selective decrease in colonic CD56~+ T and CD161~+ T cells in the inflamed mucosa of patients with ulcerative colitis[J]. Masaru Shimamoto,Yoshitaka Ueno,Shinji Tanaka,Toshiko Onitake,Rie Hanaoka,Kyoko Yoshioka,Tsuyoshi Hatakeyama,Kazuaki Chayama.World Journal of Gastroenterology. 2007(45)
[2]  
Influence of dexamethasone on inflammatory mediators and NF-κB expression in multiple organs of rats with severe acute pancreatitis[J]. Xi-Ping Zhang, Department of General Surgery, Hangzhou First People’s Hospital, Hangzhou 310006, Zhejiang Province, China Ling Zhang, Class s0201 of Seven Year’s Clinical Medicine, Shanxi Medical University, Taiyuan 310001, Shanxi Province, China Lin-Jie Chen, Zhejiang University of Traditional Chinese Medical, Hangzhou 310053, Zhejiang Province, China Qi-Hui Ch
[3]   Increased DNA binding activity of NF-κB,STAT-3,SMAD3 and AP-1 in acutely damaged liver [J].
Adriana Salazar-Montes ;
Luis Ruiz-Corro ;
Ana Sandoval-Rodriguez ;
Alberto Lopez-Reyes ;
Juan Armendariz-Borunda .
World Journal of Gastroenterology, 2006, (37) :5995-6001
[4]   Augmented regeneration of partial liver allograft induced by nuclear factor-kB decoy oligodeoxynucleotides-modified dendritic cells [J].
Ming-Qing Xu Yu-Ping Suo Jian-Ping Gong Ming-Man Zhang Lü-Nan Yan Department of General Surgery .
World Journal of Gastroenterology, 2004, (04) :573-578
[5]  
Human B lymphoblast cell lines defective of Stat6 signaling producehigh levels of proinflammatory cytokines IL-12, TNFα and IFNγ[J] . Wen Zhang,Walter Koltun,Jennifer Thompson,Anna Tilberg,Eva Galka,Lisa Poritz,Michael Chorney.International Journal of Oncology . 2004 (2)
[6]   Inflammatory bowel disease [J].
Podolsky, DK .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (06) :417-429
[7]  
Role of Cytokines in the Pathogenesis of Inflammatory Bowel Disease[J] . Konstantinos A. Papadakis,Stephan R. Targan.Annual Review of Medicine . 2000
[8]  
TUMOR NECROSIS FACTOR RECEPTOR AND Fas SIGNALING MECHANISMS[J] . D. Wallach,E. E. Varfolomeev,N. L. Malinin,Yuri V. Goltsev,A. V. Kovalenko,M. P. Boldin.Annual Review of Immunology . 1999 (1)
[9]  
Interleukin4regu-lates phosphorylation of serine756inthe transactivation domain of Stat6.Roles for multiple phosphorylation sites and Stat6function .2 Wang Y,Malabarba MG,Nagy ZS,et al. J Biol Chem . 2004