详细信息
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
Effect of HMGB1 on MyD88 and NF-κB in Syndrome Ulcerative Colitis Rats by Shaoyaotang
文献类型:期刊文献
中文题名: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
英文题名:Effect of HMGB1 on MyD88 and NF-κB in Syndrome Ulcerative Colitis Rats by Shaoyaotang
作者:王移飞[1];王凤仪[1];徐兰萍[1];李丽霞[1];蒲晓薇[1];祖健[1];赵党生[1]
第一作者:王移飞
机构:[1]甘肃中医药大学
第一机构:甘肃中医药大学
年份:2018
卷号:24
期号:12
起止页码:86
中文期刊名:中国实验方剂学杂志
外文期刊名:Chinese Journal of Experimental Traditional Medical Formulae
收录:CSTPCD;;北大核心:【北大核心2017】;CSCD:【CSCD_E2017_2018】;
基金:国家自然科学基金项目(8150150228)
语种:中文
中文关键词:芍药汤;溃疡性结肠炎;湿热型;高迁移率族蛋白B1(HMGB1);衔接蛋白髓样分化因子88(MyD88);核转录因子-κB(NF-κB)
外文关键词:Shaoyaotang;ulcerative colitis;damp-heat type;high mobility group protein B1 ( HMGB1 );adapter protein myeloid differentiation factor 88 (MyD88);nuclear transcription factor-κB (NF-κB)
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(My D88)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,My D88,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,My D88,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My D88,NF-κB基因表达,减弱湿热型UC的炎症反应。
Objective: To observe the effect of Shaoyaotang on the expression of high mobility group protein B1( HMGB1),adapter protein myeloid differentiation factor 88( My D88) 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 2,4,6-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,My D88 and NF-κB were significantly increased in the model group( P〈0. 05). As compared with the model group,the expressions of HMGB1,My D88,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 My D88 and NF-κB in TLRs signaling pathway and reduce the inflammatory reaction of damp-heat type UC.
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