PDF(Pubmed)
Abstract：
In traditional Korean medicine, the 16-herb concoction Bojanggunbi-tang (BGT) is used to treat various gastrointestinal (GI) diseases. In this study, we investigated the regulatory mechanism underlying the influence of BGT on the interstitial cells of Cajal (ICCs), pacemaker cells in the GI tract. Within 12 h of culturing ICCs in the small intestines of mice, the pacemaker potential of ICCs was recorded through an electrophysiological method. An increase in the BGT concentration induced depolarization and decreased firing frequency. This reaction was suppressed by cholinergic receptor muscarinic 3 (CHRM3) antagonists, as well as 5-hydroxytryptamine receptor (5HTR) 3 and 4 antagonists. Nonselective cation channel inhibitors, such as thapsigargin and flufenamic acid, along with protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) inhibitors, also suppressed the BGT reaction. Guanylate cyclase and protein kinase G (PKG) antagonists inhibited BGT, but adenylate cyclase and protein kinase A antagonists had no effect. In conclusion, we demonstrated that BGT acts through CHRM3, 5HTR3, and 5HTR4 to regulate intracellular Ca2+ concentrations and the PKC, MAPK, guanylate cycle, and PKG signaling pathways.
摘要：
在韩国传统医学中，16-草药混合物Bojanggunbi-tang（BGT）用于治疗各种胃肠道（GI）疾病。在这项研究中,我们研究了BGT对Cajal间质细胞（ICCs）影响的调节机制，胃肠道中的起搏器细胞。在小鼠小肠中培养ICC的12小时内，通过电生理学方法记录ICC的起搏器电位.BGT浓度的增加会引起去极化并降低点火频率。该反应被胆碱能受体毒蕈碱3（CHRM3）拮抗剂抑制，以及5-羟色胺受体（5HTR）3和4拮抗剂。非选择性阳离子通道抑制剂，如thapsigargin和氟芬那酸，以及蛋白激酶C（PKC）和丝裂原活化蛋白激酶（MAPK）抑制剂，也抑制了BGT反应。鸟苷酸环化酶和蛋白激酶G（PKG）拮抗剂抑制BGT，但腺苷酸环化酶和蛋白激酶A拮抗剂没有效果。总之,我们证明了BGT通过CHRM3，5HTR3和5HTR4来调节细胞内Ca2浓度和PKC，MAPK,鸟苷酸循环，和PKG信号通路。
