首页> 外文OA文献 >Qingchang Wenzhong Decoction Ameliorates Dextran Sulphate Sodium-Induced Ulcerative Colitis in Rats by Downregulating the IP10/CXCR3 Axis-Mediated Inflammatory Response
【2h】

Qingchang Wenzhong Decoction Ameliorates Dextran Sulphate Sodium-Induced Ulcerative Colitis in Rats by Downregulating the IP10/CXCR3 Axis-Mediated Inflammatory Response

机译:青昌汤汤通过下调IP10 / CXCR3轴介导的炎症反应来改善大鼠硫酸甲酸钠钠诱导的溃疡性结肠炎

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Qingchang Wenzhong Decoction (QCWZD) is an effective traditional Chinese medicine prescription. Our previous studies have shown that QCWZD has significant efficacy in patients with mild-to-moderate ulcerative colitis (UC) and in colonic mucosa repair in UC rat models. However, the exact underlying mechanism remains unknown. Thus, this study was conducted to determine QCWZD’s efficacy and mechanism in dextran sulphate sodium- (DSS-) induced UC rat models, which were established by 7-day administration of 4.5% DSS solution. QCWZD was administered daily for 7 days, after which the rats were euthanized. Disease activity index (DAI), histological score (HS), and myeloperoxidase (MPO) level were determined to evaluate UC severity. Serum interferon gamma-induced protein 10 (IP10) levels were determined using ELISA kits. Western blotting and real-time polymerase chain reaction were, respectively, used to determine colonic protein and gene expression of IP10, chemokine (cys-x-cys motif) receptor (CXCR)3, and nuclear factor- (NF-) κB p65. Intragastric QCWZD administration ameliorated DSS-induced UC, as evidenced by decreased DAI, HS, and MPO levels. Furthermore, QCWZD decreased the protein and gene expression of IP10, CXCR3, and NF-κB p65. Overall, these results suggest that QCWZD ameliorates DSS-induced UC in rats by downregulating the IP10/CXCR3 axis-mediated inflammatory response and may be a novel UC therapy.
机译:清肠文忠汤(QCWZD)是一种有效的传统中国中药处方。我们先前的研究已经表明,QCWZD有轻度至中度溃疡性结肠炎(UC)和结肠黏膜修复的UC大鼠模型显著疗效。然而,确切的作用机制尚不清楚。因此,本研究是为了确定QCWZD在硫酸葡聚糖钠(DSS-)诱导的UC大鼠模型的疗效和机制,这是由4.5%DSS溶液7天的给药建立。 QCWZD每天给予7天,之后将大鼠安乐死。疾病活动指数(DAI),组织学评分(HS),和髓过氧化物酶(MPO)水平进行了测定,以评估UC严重性。血清干扰素γ诱导的蛋白10(IP10)水平用ELISA试剂盒测定。 Western印迹和实时聚合酶链反应分别为用于确定结肠蛋白和IP10的基因表达,趋化因子(CYS-X-半胱氨酸基序)受体(CXCR)3,和核因子(NF-)κBP65。胃内给药QCWZD改善DSS诱导的UC,就证明了减少DAI,HS,和MPO水平。此外,QCWZD下降IP10,CXCR3,和NF-κB的p65蛋白和基因的表达。总体而言,这些结果表明,QCWZD改善DSS诱导的UC大鼠通过下调的IP10 / CXCR3轴介导的炎症反应,并且可以是一种新颖的UC治疗。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号