Xiang-Qi-Tang and its active components exhibit anti-inflammatory and anticoagulant properties by inhibiting MAPK and NF-κB signaling pathways in LPS-treated rat cardiac microvascular endothelial cells
Xiang-Qi-Tang and its active components exhibit anti-inflammatory and anticoagulant properties by inhibiting MAPK and NF-κB signaling pathways in LPS-treated rat cardiac microvascular endothelial cells
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DOI：
10.3109/08923973.2012.744034
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发表时间：
2013-04-01
影响因子：
3.3
通讯作者：
Fu, Ben-Dong
中科院分区：
文献类型：
--
作者：
He, Chang-Liang;Yi, Peng-Fei;Fu, Ben-Dong
香芪汤是由香附、黄芪、穿心莲组成的中药复方。α-香附酮（α-Cyperone，α-Cyperone）、甘草苷IV（AS-IV）和穿心莲内酯（andrographylaxis，AND）是该配方中的三种主要活性成分。XQT可以调节炎症或凝血反应。因此，我们评估XQT对脂多糖（LPS）诱导的大鼠心脏微血管内皮细胞（RCMECs）炎症模型的影响。XQT、KLF、AS-IV和AND可抑制肿瘤坏死因子α（TNF-α）、细胞间粘附分子-1（ICAM-1）和纤溶酶原激活物抑制剂-1（派-1）的产生，上调Kruppel样因子2（KLF 2）的mRNA表达。XQT和THP可抑制组织因子（TF）的分泌。为进一步探讨其作用机制，我们发现XQT或其活性成分β 1-D、AS-IV和AND可显著抑制LPS刺激的RCMECs中细胞外信号调节激酶（ERK）、c-jun氨基末端激酶（JNK）和p38磷酸化蛋白的表达，并降低核因子κ B（NF-kappa B）p65蛋白的磷酸化水平。提示XQT及其活性成分通过丝裂原活化蛋白激酶（MAPK）和NF-κ B B信号通路抑制炎症和凝血介质的表达。这些发现可能有助于进一步研究该配方的作用机制，以及炎症或凝血相关疾病的治疗。
Xiang-Qi-Tang (XQT) is a Chinese herbal formula containing Cyperus rotundus, Astragalus membranaceus and Andrographis paniculata. Alpha-Cyperone (CYP), astragaloside IV (AS-IV) and andrographolide (AND) are the three major active components in this formula. XQT may modulate the inflammatory or coagulant responses. We therefore assessed the effects of XQT on lipopolysaccharide (LPS)-induced inflammatory model of rat cardiac microvascular endothelial cells (RCMECs). XQT, CYP, AS-IV and AND inhibited the production of tumor necrosis factor alpha (TNF-alpha), intercellular cell adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1), and up-regulated the mRNA expression of Kruppel-like factor 2 (KLF2). XQT and CYP inhibited the secretion of tissue factor (TF). To further explore the mechanism, we found that XQT, or its active components CYP, AS-IV and AND significantly inhibited extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK) and p38 phosphorylation protein expression as well as decreased the phosphorylation levels of nuclear factor kappa B (NF-kappa B) p65 proteins in LPS-stimulated RCMECs. These results suggested that XQT and its active components inhibited the expression of inflammatory and coagulant mediators via mitogen-activated protein kinase (MAPKs) and NF-kappa B signaling pathways. These findings may contribute to future research on the action mechanisms of this formula, as well as therapy for inflammation- or coagulation-related diseases.