久泻灵颗粒对脾肾阳虚型溃疡性结肠炎大鼠结肠髓样分化因子88和白细胞介素受体相关激酶1表达影响.docVIP

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久泻灵颗粒对脾肾阳虚型溃疡性结肠炎大鼠结肠髓样分化因子88和白细胞介素受体相关激酶1表达影响.doc

久泻灵颗粒对脾肾阳虚型溃疡性结肠炎大鼠结肠髓样分化因子88和白细胞介素受体相关激酶1表达影响

久泻灵颗粒对脾肾阳虚型溃疡性结肠炎大鼠结肠髓样分化因子88和白细胞介素受体相关激酶1表达的影响   摘要:目的 观察久泻灵颗粒对脾肾阳虚型溃疡性结肠炎(UC)大鼠结肠髓样分化因子88(MyD88)和白细胞介素受体相关激酶1(IRAK1)表达的影响,探讨其作用机制。方法 采用复合方法制作动物模型。90只Wistar大鼠随机分为空白组、模型组、阳性药组和久泻灵高、中、低剂量组,各给药组给予相应药物灌胃。RT-qPCR、免疫组化和Western blot分别检测MyD88、IRAK1基因和蛋白的表达。结果 与空白组比较,模型组大鼠MyD88、IRAK1基因和蛋白表达均增强(P0.01);与模型组比较,各给药组大鼠MyD88、IRAK1基因和蛋白表达均减弱(P0.01),久泻灵颗粒高剂量组最为明显。结论 久泻灵颗粒可抑制MyD88、IRAK1的表达,影响MyD88信号通路的传导,阻滞下游炎症因子的释放,从而达到治疗脾肾阳虚型UC的目的。   关键词:久泻灵颗粒;溃疡性结肠炎;脾肾阳虚;髓样分化因子88;白细胞介素受体相关激酶1;大鼠   DOI:10.3969/j.issn.1005-5304.2017.09.013   中图分类号:R285.5 文献标识码:A 文章编号:1005-5304(2017)09-0051-04   Effects of Jiuxieling Granules on Expressions of MyD88 and IRAK1 in Ulcerative Colitis Rats with Spleen-Kidney Yang Deficiency LIU Xiang-yu1, LIU Yong-hua1, LI Hai-long1,2, LIU Feng-lin1, CHENG Xiao-li1, WU Yu-hong1,2 (1. Gansu University of Chinese Medicine, Lanzhou 730000, China; 2. Gansu Province Chinese Medicine New Products Engineering Laboratory, Lanzhou 730000, China)   Abstract: Objective To observe the effects of Jiuxieling Granules on the expressions of MyD88 and IRAK1 in ulcerative colitis model rats with spleen-kidney yang deficiency; To discuss its mechanism of action. Methods Animal models were established by compound methods. 90 Wistar rats were randomly divided into blank group, model group, positive medicine group, and Jiuxieling Granules high-, medium-, and low-dose groups. Each administration group was given relevant medicine for gavage. RT-qPCR, SP immunohistochemistry and Western blot were used to detect mRNA and proteins of MyD88 and IRAK1 in colon tissues. Results Compared with the blank group, mRNA and proteins of MyD88 and IRAK1 in the model group increased (P0.01). Compared with the model group, mRNA and proteins of MyD88 and IRAK1 in each administration group decreased (P0.01), especially in Jiuxieling Granules high-dose group. Conclusion Jiuxieling Granules can reduce the expressions of MyD88 and IRAK1, and then influence the transmission of MyD88 signaling pathway and bloc

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