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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Da-Cheng-Qi Decoction Alleviates Intestinal Injury in Rats with Severe Acute Pancreatitis by Inhibiting the JAK2-STAT3 Signaling Pathway
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Da-Cheng-Qi Decoction Alleviates Intestinal Injury in Rats with Severe Acute Pancreatitis by Inhibiting the JAK2-STAT3 Signaling Pathway

机译:Da-Cheng-Qi汤剂通过抑制JAK2-STAT3信号通路,减轻了严重急性胰腺炎的大鼠肠损伤

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Objective. To investigate the effect of Da-Cheng-Qi decoction (DCQD) on treating intestinal injury in rats with severe acute pancreatitis (SAP), based on the Janus kinase 2 (JAK2)/signal transducers and transcription 3 (STAT3) signaling pathway. Methods. Rats were randomly divided into the SAP group, SAP?+?ruxolitinib (JAK2 inhibitor) group, SAP?+?Stattic (STAT3 inhibitor) group, SAP?+?DCQD group, and sham operation group. They were further divided into 3-hour, 6-hour, 12-hour, and 18-hour subgroups. Levels of amylase and the inflammatory cytokines tumor necrosis factor-α, interleukin 6, interleukin 10, and interleukin 4 in plasma were tested. The messenger ribonucleic acid (mRNA) expression of JAK2 and STAT3 and the protein expression of phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) in the pancreas and terminal ileum tissues were examined. Results. Rats with SAP had severe changes in plasma levels of amylase and inflammatory cytokines and showed an overexpression of JAK2 mRNA, STAT3 mRNA, p-JAK2 protein, and p-STAT3 protein in the pancreas and terminal ileum. The events could be downregulated by treatment with DCQD, JAK2 inhibitor, and STAT3 inhibitor. Conclusions. In rats with SAP, DCQD ameliorated inflammatory cytokines and intestinal injury, which may be closely associated with the inhibition of the JAK2/STAT3 signaling pathway.
机译:客观的。基于Janus激酶2(JAK2)/信号传感器和转录3(STAT3)信号通路,探讨大程芪汤(DCQD)对大鼠治疗严重急性胰腺炎(SAP)肠损伤的影响。方法。将大鼠随机分为SAP组,SAP?+?ruxolitinib(JAK2抑制剂)组,SAP?+?Stattic(STAT3抑制剂)组,SAP?+?DCQD组和假手术组。它们进一步分为3小时,6小时,12小时和18小时的亚组。测试淀粉酶和炎症细胞因子肿瘤坏死因子-α,白细胞介素6,白细胞介素10和血浆中白细胞介素4。研究了JAK2和STAT3的信使核糖核酸(mRNA)表达以及磷酸化的JAK2(P-JAK2)和磷酸化STAT3(P-STAT3)的蛋白表达在胰腺和末端感应组织中。结果。 SAP的大鼠具有血浆酶和炎性细胞因子的血浆水平的严重变化,并且在胰腺和末端HELEUM中显示了JAK2 mRNA,STAT3 mRNA,P-JAK2蛋白和P-Stat3蛋白的过表达。这些事件可以通过用DCQD,JAK2抑制剂和Stat3抑制剂治疗来降低。结论。在具有SAP的大鼠中,DCQD改善炎性细胞因子和肠损伤,其可能与JAK2 / Stat3信号传导途径的抑制密切相关。

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