湿热对溃疡性结肠炎大鼠模型影响的实验研究
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摘要
目的:探讨湿热对溃疡性结肠炎(UC)大鼠模型的影响。方法:采用内因(高脂高糖饮食)和外因(高湿高温气候)因素刺激,再辅以DNCB/乙酸灌肠建立湿热UC大鼠模型,探讨湿热对UC大鼠证候学、病理学及免疫学指标的变化。结果:湿热UC比单纯UC更早出现与大肠湿热UC患者相似的临床症状,DAI、病理学评分均升高;湿热UC血清SOD、MPO、MIF和组织TXB_2水平明显高于单纯UC(P<0.05);湿热UC血清和组织MPO、P选择素、组织MIF、TXB_2与单纯UC表达水平一致,均比正常组升高。结论:血清SOD、MPO、MIF和组织TXB_2水平可作为判断湿热病因所致UC的免疫标识物;湿热能促进UC的发生和进一步加重炎症程度,是UC的主要病因。
Objective:To investigate effects of damp-heat on ulcerative colitis(UC) rat model.Methods:The damp-heat UC rat model was established with the environment of internal(high-fat and high-sugar diet) and external(high temperature and high temperature climate) stimulations,supplemented by DNCB/acetic acid enema.In this study,we investigated the changes of syndromes,pathology and immunology of damp-heat in UC rats.Results:Compared with the UC group,clinical symptoms in damp-heat UC group appeared earlier with the clinical symptoms similar to those of large intestine damp-heat UC patients.Their scores of DAI and pathology became higher.Their levels of SOD,MPO and MIF in serum and TXB_2 in tissue were significantly higher than simple UC(P<0.05).Moreover,their expressions of MPO,P-selectin in serum or tissue,and MIF,TXB_2 in tissue were consistent with UC alone,which were higher than those of the normal group.Conclusion:The levels of SOD,MPO,MIF in serum and TXB_2 in tissue can be used as immune markers to determine the cause of damp-heat UC.Damp-heat is the main cause of UC which can promote the occurrence of UC and further increase the degree of inflammation.
Objective:To investigate effects of damp-heat on ulcerative colitis(UC) rat model.Methods:The damp-heat UC rat model was established with the environment of internal(high-fat and high-sugar diet) and external(high temperature and high temperature climate) stimulations,supplemented by DNCB/acetic acid enema.In this study,we investigated the changes of syndromes,pathology and immunology of damp-heat in UC rats.Results:Compared with the UC group,clinical symptoms in damp-heat UC group appeared earlier with the clinical symptoms similar to those of large intestine damp-heat UC patients.Their scores of DAI and pathology became higher.Their levels of SOD,MPO and MIF in serum and TXB_2 in tissue were significantly higher than simple UC(P<0.05).Moreover,their expressions of MPO,P-selectin in serum or tissue,and MIF,TXB_2 in tissue were consistent with UC alone,which were higher than those of the normal group.Conclusion:The levels of SOD,MPO,MIF in serum and TXB_2 in tissue can be used as immune markers to determine the cause of damp-heat UC.Damp-heat is the main cause of UC which can promote the occurrence of UC and further increase the degree of inflammation.
引文
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[2] Jiang YF,Huang ZX,et al.Study on Treatment of Ulcerative Colitis with Damp-heat Syndrome[J].Chin ARCH of Tradit Chin Med,2004,22(1):116-119.
[3] Yang GF,Wang JZ.Investigation on TCM Syndrome of 97 Patients with Ulcerative Colitis[J].Henan Trad Chin Med,2008,28(12):56-57.
[4] Zhang LF.Discuss the Chinese medicine disease name and the pathogenesis of ulcerative colitis[J].Forum on Trad Chin Med,2009,24(3):9-10.
[5] 石洋,白光.从六淫致病之“湿热为患”谈溃疡性结肠炎[J].中医药临床,2017,29(9):1399-1401.
[6] 翁一洁,郑学宝.湿热型溃疡性结肠炎大鼠模型的建立与研究[J].时珍国医国药,2011,22(10):2522-2525.
[7] 翁一洁,郑学宝.大鼠内因湿热造模方法研究[J].时珍国医国药,2010,21(2):479-480.
[8] Zhang Q,Tao H,Lin Y,et al.A superoxide dismutase/catalase mimetic nanomedicine for targeted therapy of inflammatory bowel disease[J].Biomaterials,2016,10(105):206-221.
[9] 佟丽,吴仕九,陈江华,等.湿热证病人免疫功能与自由基水平变化的研究[J].中国实验临床免疫学杂志,1999,11(4):176-178.
[10] Egresi A,Kovács á,Szilvás á,Blázovics A.Gut-liver axis in inflammatory bowel disease.A retrospective study[J].Orvosi hetilap,2017,158(26) :1014-1021.
[11] Mohammadi E,Qujeq D,Taheri H,et al.Evaluation of Serum Trace Element Levels and Superoxide Dismutase Activity in Patients with Inflammatory Bowel Disease:Translating Basic Research into Clinical Application[J].Biological trace element research,2017,177(2):235-240.
[12] Pawlica-Gosiewska D,Solnica B,Gawlik K,et al.The use of selected neutrophil protein plasma concentrations in the diagnosis of Crohn′s disease and ulcerative colitis a preliminary report[J].Postepy Hig Med Dosw,2017,1(10):243-253.
[13] Liu G,Yu L,Fang J,et al.Methionine restriction on oxidative stress and immune response in dss-induced colitis mice[J].Oncotarget,2017,8(27):44511-44520.
[14] Ajdukovic J,Salamunic I,Hozo I,et al.Soluble P-selectin glycoprotein ligand-a possible new target in ulcerative colitis[J].Bratisl Lek Listy,2015,116(3):147-149.
[15] Yukitake H,Takizawa M,Kimura H.Macrophage Migration Inhibitory Factor as an Emerging Drug Target to Regulate Antioxidant Response Element System[J].Oxid Med Cell Longev,2017,2017:8584930.
[16] Yang,Li,Zhang.Meta-analysis of macrophage migration inhibitory factor (MIF) gene-173G/C polymorphism and inflammatory bowel disease (IBD) risk[J].International journal of clinical and experimental medicine,2017,8(6) :9570-9574.
[17] Nishihira.Molecular function of macrophage migration inhibitory factor and a novel therapy for inflammatory bowel disease[J].Annals of the New York Academy of Sciences,2012, 1271(1):53-57.
[18] Alabed Y,VanPatten S.MIF as a disease target:ISO-1 as a proof-of-concept therapeutic[J].Future Med Chem,2011,3(1):45-63.
[19] Horikawa N,Suzuki T,Uchiumi T,et al.Cyclic AMP-dependent Cl- secretion induced by thromboxane A2 in isolated human colon[J].The Journal of physiology,2005,562(Pt 3):885-897.
[20] Müller G,Taube C,Senger U,et al.Thromboxane analyses in patients with chronic inflammatory bowel diseases[J].Dtsch Z Verdau Stoffwechselkr,1986,46(4):243-246.
[21] Di Sabatino A,Santilli F,Guerci M,et al.Oxidative stress and thromboxane-dependent platelet activation in inflammatory bowel disease:effects of anti-TNF-α treatment[J].Thromb Haemost,2016,116(3):486-495.