Effect of Shaoyaotang on Expressions of AP-1 and TNF-<italic style="font-style: italic">α</italic> in Colon of Rats with Hygrothermal Ulcerative Colitis

Feng-yi WANG; Dang-sheng ZHAO; Xiao-wei PU; Jian ZU; Min XU; Chen-an SUN

doi:10.13422/j.cnki.syfjx.20191603

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Effect of Shaoyaotang on Expressions of AP-1 and TNF-α in Colon of Rats with Hygrothermal Ulcerative Colitis

Classic Prescriptions | 更新时间：2021-02-09

- Effect of Shaoyaotang on Expressions of AP-1 and TNF-α in Colon of Rats with Hygrothermal Ulcerative Colitis
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 16, Pages: 7-11(2019)
- 作者机构：
  
  甘肃中医药大学，兰州　 730000
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191603
  CLC： R2-0; R22; R285.5; R289
- Received：03 December 2018，
  
  Published Online：08 May 2019，
  
  Published：20 August 2019
- 稿件说明：
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Feng-yi WANG, Dang-sheng ZHAO, Xiao-wei PU, et al. Effect of Shaoyaotang on Expressions of AP-1 and TNF-α in Colon of Rats with Hygrothermal Ulcerative Colitis[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(16): 7-11.
DOI：

Feng-yi WANG, Dang-sheng ZHAO, Xiao-wei PU, et al. Effect of Shaoyaotang on Expressions of AP-1 and TNF-α in Colon of Rats with Hygrothermal Ulcerative Colitis[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(16): 7-11. DOI： 10.13422/j.cnki.syfjx.20191603.

摘要

目的：

观察芍药汤对湿热内蕴型溃疡性结肠炎(UC)大鼠模型结肠组织中激活蛋白-1(AP-1)与肿瘤坏死因子-

(TNF-

)的基因及蛋白表达的影响，探讨芍药汤治疗UC的作用机制。

方法：

将60只Wistar大鼠随机分为正常组、模型组、柳氮磺砒啶组及芍药汤低、中、高剂量组，采用病症结合的方法复制湿热内蕴型UC大鼠模型，即高脂高糖辛辣食物及免疫复合法，联合2，4，6-三硝基苯磺酸(TNBS)结合乙醇复合法。造模成功后，分别给予芍药汤低、中、高(6，12，24 g·kg

－1

)灌胃，柳氮磺胺嘧啶1 g·kg

－1

剂量灌胃，正常组给予等体积生理盐水，连续21 d。实时荧光定量聚合酶链式反应(Real-time PCR)检测结肠组织AP-1，TNF-

mRNA表达，蛋白免疫印迹法(Western blot)检测结肠组织AP-1，TNF-

蛋白表达。

结果：

与正常组比较，模型组AP-1，TNF-

mRNA及蛋白相对表达量明显升高(

0.05)；与模型组比较，各干预组AP-1，TNF-

mRNA及蛋白表达量明显下降(

0.05)，以芍药高剂量组较为明显。

结论：

芍药汤可抑制湿热型UC大鼠AP-1蛋白刺激TNF-

的表达，可能是其治疗湿热型UC的机制之一。

Abstract

Objective:

To observe the effect of Shaoyaotang on mRNA and protein expressions of colon tissue activated protein-1 (AP-1) and tumor necrosis factor-

(TNF-

) of hot and humid-type intrinsic ulcerative colitis (UC) model in rats

in order to explore the mechanism of action of herbaceous peony decoction in the treatment of UC.

Method:

Totally 60 Wistar rats were randomly divided into blank group

model group

SASP group

and low

medium and high-dose Shaoyaotang groups. The damp-heat intrinsic UC rat model was replicated based on integrated disease and syndrome

namely

high-fat and high-sugar spicy food and immune complex method combined with 2

6-trinitrobenzene sulfolnic acid (TNBS) and ethanol complex method. After the successful modeling

low

medium and high-dose Shaoyaotang (6

24 g·kg

-1

) was given by gavage

and 1 g·kg

-1

dose of salazol sulfadiazine was given to by gavage. The blank group was given constant volume normal saline for 21 d. Real-time fluorescence quantitative polymerase chain reaction(Real-time PCR) was used to detect mRNA expressions of AP-1 and TNF-

in colon tissues

and Western blot was used to detect protein expressions of AP-1 and TNF-

in colon tissues.

Result:

Compared with the blank group

relative mRNA and protein expressions of AP-1

TNF-

in the model group were significantly increased (

0.05). Compared with the model group

mRNA and protein expressions of AP-1

TNF-

in the treatment groups were significantly decreased (

0.05).

Conclusion:

Shaoyaotang can inhibit the expression of TNF-

and stimulate AP-1 protein expression in rats with damp-heat UC.

关键词

Keywords

references

Burisch J , Munkholm P . The epidemiology of inflammatory bowel disease [J]. Scand J Gastroenterol , 2015 , 50 ( 8 ): 942 - 951 .

Wagner E F . Bone development and inflammatory disease is regulated by AP-1 (Fos/Jun) [J]. Ann Rheum Dis , 2010 , 69 : 86 - 88 .

Thomsen M K , Bakiri L , Hasenfuss S C , et al . JUNB/AP-1 controls IFN-γ during inflammatory liver disease [J]. Eur J Clin Invest , 2013 , 123 ( 12 ): 5258 - 5268 .

刘启鸿，黄文彬，骆云丰，等．溃疡性结肠炎当重湿热 [J]．陕西中医药大学学报， 2018 ， 41 ( 6 )： 13 - 16 ．

王移飞，王凤仪，徐兰萍，等．芍药汤经HMGB1调节湿热型溃疡性结肠炎大鼠MyD88和NF-κB的分子机制 [J]．中国实验方剂学杂志， 2018 ， 24 ( 12 )： 86 - 91 ．

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 ．

万明民，杜悦，陈纯苇，等．芍药汤的临床应用及实验研究进展 [J]．中国中医药现代远程教育， 2018 ， 16 ( 23 )： 154 - 157 ．

刘琦，罗霞，罗爽，等．芍药苷通过抑制NLRP3炎症小体治疗溃疡性结肠炎小鼠的研究 [J]．中药新药与临床药理， 2018 ， 29 ( 4 )： 409 - 414 ．

罗爽，罗霞，刘琦，等．大黄酸对DSS诱导溃疡性结肠炎小鼠的治疗作用及机制探讨 [J]．中国实验方剂学杂志， 2017 ， 23 ( 11 )： 109 - 113 ．

Nielsen O H , Bjerrum J T , Herfarth H H , et al . Recent advances using immunomodulators for inflammatory bowel disease [J]. J Clin Pharmacol , 2013 , 53 ( 6 ): 575 - 588 .

Danese S . New therapies for inflammatory bowel disease: from the bench to the bedside [J]. Gut , 2012 , 61 : 918 - 932 .

CHEN Y , Currie R W . Small interfering RNA knocks down heat shock factor-1 (HSF-1) and exacerbatespro-inflammatory activation of NF-kappa B and AP-1 in vascular smooth muscle cells [J]. Cardiovasc Res , 2006 , 69 : 66 - 75 .

CHANG L , Karin M . Mammalian MAP kinase signalling cascades [J]. Nature , 2001 , 410 ( 6824 ): 37 - 40 .

Johnson G L , Lapadat R . Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases [J]. Science , 2002 , 298 ( 5600 ): 1911 - 1912 .

陈维雄，陆允敏，陈金联，等． AP-1在小鼠实验性肠炎中的表达 [C]// 中华医学会．第七次全国消化病学术会议论文汇编(下册)：2007年卷．济南：出版社不详， 2007 ： 188 ．

Park S , Regmi S C , Park S Y , et al . Protective effect of 7-O-succinyl macrolactin A against intestinal inflammation is mediated through PI3-kinase/Akt/mTOR and NF-κB signaling pathways [J]. Eur J Pharmacol , 2014 , 735 : 184 - 192 .

王彤，王骁，范焕芳，等．白头翁汤对溃疡性结肠炎模型小鼠结肠黏膜及血清TNF-α，IL-6影响 [J]．辽宁中医药大学学报， 2017 ， 19 ( 2 )： 32 - 35 ．

易文，陈置丰，石孟琼，等．左金丸阻断溃疡性结肠炎小鼠NF-κB激活MIF，TNF-α及IL-1β，IL-6表达 [J]．中药药理与临床， 2014 ， 30 ( 6 )： 9 - 13 ．

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Effect of Shaoyaotang on Expressions of AP-1 and TNF-α in Colon of Rats with Hygrothermal Ulcerative Colitis

DOI：10.13422/j.cnki.syfjx.20191603

摘要

Abstract

关键词

Keywords

references