首页|嘎木珠尔灌肠通过对IL-6/STAT3信号通路的调节而改善结肠炎模型大鼠的结肠炎症

嘎木珠尔灌肠通过对IL-6/STAT3信号通路的调节而改善结肠炎模型大鼠的结肠炎症

Gamuzhuer Ameliorate Colonic Lesions of Colitis Model Rats by Regulating IL-6/STAT3 Signal Pathway

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目的:观察嘎木珠尔灌肠对结肠炎模型大鼠结肠病变的影响;并研究其对IL-6/STAT3信号通路的调节作用.方法:40只大鼠被随机分组;空白组、造模组、柳氮磺吡啶组及嘎木珠尔组,每组10只.以乙醇/TNBS灌肠造模后分别以生理盐水、柳氮磺吡啶及嘎木珠尔灌肠.14天后对结肠大体形态及结肠病理切片进行观察,免疫组化分析结肠IL-6及STAT3的表达.结果:造模后结肠大体评分及组织病理评分均显著增高(P均<0.01);结肠IL-6及STAT3阳性染色细胞数量均显著增多(P均<0.01).经柳氮磺吡啶及嘎木珠尔治疗后结肠大体评分均明显降低(P<0.01、P<0.05);结肠组织病理评分均显著降低(P均<0.01);结肠IL-6及STAT3阳性染色细胞数均显著减少(P均<0.01).结论:嘎木珠尔灌肠能减轻结肠炎模型大鼠的结肠炎症,并可改善其病理结构的破坏.其可能通过对IL-6/STAT3信号通路下调而发挥作用.
Objective:To observe the improvement effect of Gamuzhuer enema on colonic lesions of colitis model rats,and to study its effect on IL-6/STAT3 signaling pathway.Methods:40 rats were divided at random into 4 groups:blank,model,sulfasalazine and Gamuzhuer,with 10 in each group.After the model was made by ethanol/TNBS enema;normal saline,sulfasalazine and Gamuzhuer enema were used respectively.After 14 days,the colon was taken for observation with naked eye and microscope.Immunohistochemical analysis was performed to evaluate the expression of IL-6 and STAT3 in colon.Results:After modeling,obvious increases in gross score(P<0.01),histopathological score(P<0.01),expressions of IL-6 and STAT3(all P<0.01)of colon were found.After the treatment with sulfasalazine and Gamuzhuer,obvious decreases in gross score(P<0.01,P<0.05),histopathological score(all P<0.01),expressions of IL-6 and STAT3(all P<0.01)of colon were found.Conclusion:Gamuzhuer enema can reduce the colonic inflammation of colitis model rats and repair the damage of its pathological structure.It may work well in the treatment by regulating down IL-6/STAT3 signal pathway.

GamuzhuerUlcerative colitisInterleukin-6Signal transducer and activator of transcription 3

陈浩、杜阳、何和平、侯孝涛、张丹丹、赵冉

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东南大学附属中大医院江北院区,江苏 南京 210044

内蒙古自治区国际蒙医医院,内蒙古 呼和浩特 010065

嘎木珠尔 溃疡性结肠炎 白介素-6 信号转导及转录活化因子3

内蒙古自治区卫计委科研课题中国民族医药学会科研项目

2017030302020ZY333-380503

2024

中国民族医药杂志
全国中医药图书情报工委会,内蒙古中蒙医研究所

中国民族医药杂志

影响因子:0.28
ISSN:1006-6810
年,卷(期):2024.30(8)
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