ArticleTheScientificWorldJournal2013
Involvement of MAPKs and PLC pathways in modulation of pacemaking activity by So-Cheong-Ryong-Tang in interstitial cells of Cajal from murine small intestine.
Article in TheScientificWorldJournal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Network Pharmacological Analysis and Experimental Validation of the Effect ofPlants (Basel, Switzerland) · 2023Article
- Interstitial Cells of Cajal: Potential Targets for Functional Dyspepsia Treatment Using Medicinal Natural Products.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice.Frontiers in pharmacology · 2018Article
- Fermented So-Cheong-Ryong-Tang (FCY) induces apoptosis via the activation of caspases and the regulation of MAPK signaling pathways in cancer cells.BMC complementary and alternative medicine · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeInterstitial cells of Cajal (ICCs) are the pacemaker cells that generate slow waves in the gastrointestinal (GI) tract. We have aimed to investigate the effects of Socheongryong-Tang (SCRT) in ICCs from mouse's small intestine.
methodsThe whole-cell patch-clamp configuration was used to record membrane potentials from cultured ICCs. Intracellular Ca(2+) ([Ca(2+)]i) increase was studied in cultured ICCs using fura-2 AM.
resultsICCs generated pacemaker potentials in mouse's small intestine. SCRT produced membrane depolarization in current clamp mode. Y25130 (5-HT3 receptor antagonist) and RS39604 (5-HT4 receptor antagonist) blocked SCRT-induced membrane depolarizations, whereas SB269970 (5-HT7 receptor antagonist) did not. When GDP- β -S (1 mM) was in the pipette solution, SCRT did not induce the membrane depolarizations. [Ca(2+)]i analysis showed that SCRT increased [Ca(2+)]i. In the presence of PD98059 (p42/44 MAPK inhibitor), SCRT did not produce membrane depolarizations. In addition, SB203580 (p38 MAPK inhibitor) and JNK inhibitors blocked the depolarizations by SCRT in pacemaker potentials. Furthermore, the membrane depolarizations by SCRT were not inhibited by U-73122, an active phospholipase C (PLC) inhibitor, but by U-73343, an inactive PLC inhibitor.
conclusionThese results suggest that SCRT might affect GI motility by the modulation of pacemaker activity through MAPKs and PLC pathways in the ICCs.
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