首页|优化溃结方对溃疡性结肠炎大鼠结肠Toll样受体/髓样分化因子88/核转录因子κB信号通路的影响

优化溃结方对溃疡性结肠炎大鼠结肠Toll样受体/髓样分化因子88/核转录因子κB信号通路的影响

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目的 观察优化溃结方对溃疡性结肠炎(UC)大鼠结肠Toll样受体/髓样分化因子 88/核转录因子κB(TLR/MyD88/NF-κB)信号通路的影响.方法 将40 只雄性SD大鼠随机分为空白组、模型组、优化溃结方组、柳氮磺吡啶组,每组10 只.除空白组外,其余3 组均参考三硝基苯磺酸(TNBS)/乙醇二次致炎法结合束缚法建立UC气滞血瘀型大鼠模型.造模成功后优化溃结方组大鼠予优化溃结方药液1.674 g/(kg·d)灌胃,柳氮磺吡啶组大鼠予柳氮磺吡啶药液0.54 g/(kg·d)灌胃,空白组、模型组不予任何治疗.14 天后检测各组大鼠血清白细胞介素 17A(IL-17A)、IL-10、IL-22 水平,结肠组织MyD88、TLR2、TLR4、NF-κB p65 蛋白和mRNA表达水平.结果 与空白组相比,模型组血清IL-17A、IL-22 水平显著升高(P<0.05),IL-10 水平显著下降(P<0.05);与模型组相比,优化溃结方组、柳氮磺吡啶组IL-17A、IL-22 水平显著降低(P<0.05),IL-10 水平显著升高(P<0.05);优化溃结方组IL-17A、IL-22、IL-10水平与柳氮磺吡啶组比较差异无统计学意义(P>0.05).与空白组相比,模型组结肠组织MyD88、TLR2、TLR4、NF-κB p65 蛋白和mRNA表达均显著增加(P<0.05);与模型组相比,柳氮磺吡啶组、优化溃结方组 MyD88、TLR2、TLR4、NF-κB p65 蛋白和mRNA表达均显著下降(P<0.05);优化溃结方组MyD88、TLR2、TLR4、NF-κB p65 蛋白和mRNA表达与柳氮磺吡啶组比较差异均无统计学意义(P>0.05).结论 优化溃结方可能通过调节 TLR/MyD88/NF-κB信号通路,降低炎症因子水平,减轻炎症反应,修复结肠组织的超微结构,从而修复UC大鼠结肠黏膜屏障功能.
Effect of optimized Kuijie Prescription on colon tissue in ulcerative colitis rats by regulating TLR/MyD88/NF-κB sig-naling pathway
Objective To assess the effect of optimized Kuijie Prescription on colon tissue in ulcerative colitis(UC)rats by regulating Toll-like receptor(TLR)/myeloid differentiation factor 88(MyD88)/nuclear factor kappa B(NF-κB).Methods A total of 40 male Sprague-Dawley(SD)rats were randomly divided into normal group,model group,optimized Kuijie Pre-scription group and sulfasalazine group,with 10 rats in each group.Except for the blank group,the other three groups were treated with trinitrobenzene sulfonic acid(TNBS)/ethanol second-ary inflammation method combined with restraint method to estab-lish UC rat model of qi stagnation and blood stasis type.After successful modeling,a 14-day intervention was conduted in Kui-jie Prescription group(1.674 g/kg/d optimized Kuijie Prescription),sulfasalazine group(0.54 g/kg/d sulfasalazine),blank group and model group(water administration)to detect serum levels of interleukin-17A(IL-17A),IL-10,IL-22,and the protein levels of MyD88,TLR2,TLR4 and NF-κB p65 and the expression of mRNA in colon tissue of rats.Results Com-pared with blank group,the levels of IL-17A and IL-22 in model group were significantly increased(P<0.05),while the level of IL-10 was significantly decreased(P<0.05).Compared with model group,the serum levels of IL-17A and IL-22 in optimized Kuijie Prescription group and sulfasalazine group were significantly decreased(P<0.05),but the serum level of IL-10 was significantly increased(P<0.05).There was no significant difference in the serum levels of IL-17 A,IL-22 and IL-10 between optimized Kuijie Prescription group and sulfasalazine group(P>0.05).Compared with blank group,the pro-tein levels of MyD88,TLR2,TLR4,NF-κB p65 and the expression of mRNA in colon tissue in model group were significantly increased(P<0.05).Compared with model group,the protein levels of MyD88,TLR2,TLR4,NF-κB p65 and the expres-sion of mRNA in sulfasalazine group and optimized Kuijie Prescription group were significantly decreased(P<0.05).There was no significant difference in the protein levels of MyD88,TLR2,TLR4,NF-κB p65 and the expression of mRNA between opti-mized Kuijie Prescription group and sulfasalazine group(P>0.05).Conclusion Optimized Kuijie Prescription may reduce the serum level of inflammatory factors,improve the inflammatory response,and repair the ultrastructure of colon tissue by regulating the TLR/MyD88/NF-κB signaling pathway,thereby repairing the colonic mucus barrier function in UC rats.

Ulcerative colitisHerbal medicine therapyRatAnimal experimentMyeloid differentiation factor 88Toll-like receptorsNuclear factor kappa B(NF-κB)

李娜、王磊、柳越冬、吴宪树、盛天骄、沈江立、刘银环、代晓强、乔喜婷、张渭波、张帅

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陕西省咸阳市中心医院,陕西 咸阳 712000

内蒙古自治区呼伦贝尔市中蒙医院肛肠科,内蒙古 呼伦贝尔 021008

辽宁中医药大学附属第三医院,辽宁 沈阳 110005

中国人民解放军北部战区总医院中医科,辽宁 沈阳 110005

河北中医药大学,河北 石家庄 050091

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结肠炎,溃疡性 植物药疗法 大鼠 动物实验 髓样分化因子88 Toll样受体 NF-κB

陕西省中医药管理局秦创原中医药创新研发转化项目陕西省科学技术厅陕西自然科学基础研究计划项目内蒙古自治区卫生健康委员会2022年度自治区卫生健康科技计划项目内蒙古自治区科技计划项目2023年度河北省社会科学发展研究课题

2022-QCYZH-0152022JM-4892022015992022YFSH000320230204037

2024

河北中医
河北省医学情报研究所,河北省中医药学会

河北中医

CSTPCD
影响因子:0.951
ISSN:1002-2619
年,卷(期):2024.46(6)