芍药汤经HMGB调节湿热型溃疡性结肠炎大鼠MyD88和NF-B的分子机制

王移飞; 王凤仪; 徐兰萍; 李丽霞; 蒲晓薇; 祖健; 赵党生

doi:10.13422/j.cnki.syfjx.20180942

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芍药汤经HMGB调节湿热型溃疡性结肠炎大鼠MyD88和NF-B的分子机制

药理 | 更新时间：2024-01-04

- 芍药汤经HMGB调节湿热型溃疡性结肠炎大鼠MyD88和NF-B的分子机制
- Effect of HMGB on MyD88 and NF-B in Syndrome Ulcerative Colitis Rats by Shaoyaotang
- 中国实验方剂学杂志 2018年24卷第12期页码：86-91
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目（8150150228）
- DOI：10.13422/j.cnki.syfjx.20180942
  中图分类号： R285.5
- 纸质出版日期：2018
- 稿件说明：
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王移飞, 王凤仪, 徐兰萍, 等. 芍药汤经HMGB调节湿热型溃疡性结肠炎大鼠MyD88和NF-B的分子机制[J]. 中国实验方剂学杂志, 2018,24(12):86-91.

WANG Yi-fei, WANG Feng-yi, XU Lan-ping, et al. Effect of HMGB on MyD88 and NF-B in Syndrome Ulcerative Colitis Rats by Shaoyaotang[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(12): 86-91.
王移飞, 王凤仪, 徐兰萍, 等. 芍药汤经HMGB调节湿热型溃疡性结肠炎大鼠MyD88和NF-B的分子机制[J]. 中国实验方剂学杂志, 2018,24(12):86-91. DOI： 10.13422/j.cnki.syfjx.20180942.

WANG Yi-fei, WANG Feng-yi, XU Lan-ping, et al. Effect of HMGB on MyD88 and NF-B in Syndrome Ulcerative Colitis Rats by Shaoyaotang[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(12): 86-91. DOI： 10.13422/j.cnki.syfjx.20180942.

摘要

目的：观察芍药汤对湿热型溃疡性结肠炎（ulcerative colitis，UC）大鼠模型结肠组织中高迁移率族蛋白B1（high mobility group protein B1，HMGB1）的调控，分析其对衔接蛋白髓样分化因子88（MyD88）和核转录因子-κB （NF-κB）的影响，探讨芍药汤对湿热型UC的作用机制。方法： Wistar大鼠雌雄各60只，分为空白组、模型组、芍药汤高、中、低剂量组、柳氮磺砒啶组，以2，4，6-三硝基苯磺酸（TNBS）结合乙醇复合法复制湿热型UC大鼠模型，芍药汤高、中、低剂量灌胃，柳氮磺砒啶组予柳氮磺砒啶研磨成粉配置成与中药等体积液体灌胃，空白组及模型组予等体积生理盐水灌胃，连续21 d。取结肠组织，运用实时荧光定量聚合酶链式反应（Real-time，PCR）法、蛋白免疫印迹法（Western blot）检测mRNA及蛋白表达，苏伊红-木精（HE）染色观察病理切片。结果：与空白组比较，模型组HMGB1，MyD88，NF-κB蛋白及mRNA表达明显升高（P<0.05）；与模型组比较，芍药汤各组、柳氮磺砒啶组HMGB1，MyD88，NF-κB蛋白及mRNA表达均有不同程度地下降，芍药汤高剂量组及柳氮磺砒啶组最为显著（P<0.05）。结论：芍药汤可调控HMGB1抑制TLRs信号通路中MyD88，NF-κB基因表达，减弱湿热型UC的炎症反应。

Abstract

Objective: To observe the effect of Shaoyaotang on the expression of high mobility group protein B1 (HMGB1)

adapter protein myeloid differentiation factor 88(MyD88) and nuclear transcription factor-κB(NF-κB) in the colon tissues of rats with damp-heat type ulcerative colitis (UC)

and explore the mechanism of Shaoyaotang damp-heat UC intervention. Method: Sixty male and sixty female Wistar rats were divided into blank group

model group

Shaoyaotang high

medium and low dose groups

and sulfasalazine group. The rat model of damp-heat type UC was established by 2

6-trinitrobenzene sulfonic acid (TNBS) combined with ethanol. High

medium and low doses of Shaoyaotang were given by intragastric administration

and the sulfasalazine was ground into powder and configured to be filled with liquid of equal volume. The rats in the blank group and model group were given with normal saline for continuous 21 days. Then colonic tissues were harvested.The content of gene was detected by Real-time PCR

and the content of protein was detected by Western blot. The pathological sections were observed by hematoxylin-eosin (HE) staining. Result: As compared with the blank group

the protein and mRNA expressions of HMGB1

MyD88 and NF-κB were significantly increased in the model group (P<0.05). As compared with the model group

the expressions of HMGB1

MyD88

NF-κB were decreased in Shaoyaotang groups and Sulfasalazine group (P<0.05). The effect was most significant in Shaoyaotang high dose group and sulfasalazine group (P<0.05). Conclusion: Shaoyaotang can regulate HMGB1

inhibit MyD88 and NF-κB in TLRs signaling pathway and reduce the inflammatory reaction of damp-heat type UC.

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