herbs of Chelidonium majus L.
Coptisine is an alkaloid from Chinese goldthread, and acts as an efficient uncompetitive IDO inhibitor with a Ki value of 5.8 μM and an IC50 value of 6.3 μM.
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Coptisine is one of the main components of isoquinoline alkaloids in the coptidis rhizome. The effect of coptisine on allergic rhinitis has not been investigated. In this study, we report the effects and mechanisms of coptisine using monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA)-stimulated rat basophilic leukemia cells (RBL-2H3 cells) in vitro and an ovalbumin (OVA)-induced allergic rhinitis (AR) in mice. The results showed that coptisine markedly decreased the levels of β-hexosaminidase, histamine, interleukin (IL)-4, and tumor necrosis factor (TNF)-α. Coptisine also prevented morphological changes, such as restoring an elongated shape, inhibiting granule release on toluidine blue staining, and reorganizing inhibited filamentous actins (F-actin). Additionally, coptisine blocked the phosphorylation of phosphoinositide3-kinase (PI3K)/Akt (as known as protein kinase B(PKB)) in RBL-2H3 cell. Furthermore, the results showed that coptisine suppressed OVA-induced allergic rhinitis symptoms, such as nasal rubbing and OVA-specific IgE, and histamine, IL-4 and TNF-α levels in the serum of AR mice. These data suggested that coptisine should have inhibitory effects on the inflammatory responses of mast cells, and may be beneficial for the development of coptisine as a potential anti-allergic drug
allergic rhinitis; coptisine; mast cell
Coptisine Suppresses Mast Cell Degranulation and Ovalbumin-Induced Allergic Rhinitis.
Fu S1, Ni S2, Wang D3, Hong T4.
2018 Nov 21
Coptisine is a natural small-molecular compound extracted from Coptis chinensis (CC) with a history of using for thousands of years. This work aimed at summarizing coptisine’s activity and providing advice for its clinical use. We analysed the online papers in the database of SciFinder, Web of Science, PubMed, Google scholar and CNKI by setting keywords as ‘coptisine’ in combination of ‘each pivotal pathway target’. Based on the existing literatures, we find (a) coptisine exerted potential to be an anti-cancer, anti-inflammatory, CAD ameliorating or anti-bacterial drug through regulating the signalling transduction of pathways such as NF-κB, MAPK, PI3K/Akt, NLRP3 inflammasome, RANKL/RANK and Beclin 1/Sirt1. However, we also (b) observe that the plasma concentration of coptisine demonstrates obvious non-liner relationship with dosage, and even the highest dosage used in animal study actually cannot reach the minimum concentration level used in cell experiments owing to the poor absorption and low availability of coptisine. We conclude (a) further investigations can focus on coptisine’s effect on caspase-1-involved inflammasome assembling and pyroptosis activation, as well as autophagy. (b) Under circumstance of promoting coptisine availability by pursuing nano- or microrods strategies or applying salt-forming process to coptisine, can it be introduced to clinical trial.
© 2019 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
coptisine; crosstalk network; pharmacological mechanism; signalling pathways bioavailability
Coptisine from Coptis chinensis exerts diverse beneficial properties: A concise review.
Wu J1, Luo Y1, Deng D2, Su S1, Li S3, Xiang L1, Hu Y1, Wang P1, Meng X1.
Coptisine is a natural occurring isoquinoline alkaloid isolated from the traditional Chinese medicinal herb Rhizoma coptidis. Coptisine has been reported to have protective effects on reperfusion injury in cardiomyocytes, however, the underlying mechanism remains uncertain. Here, we used a hypoxia/reoxygenation (H/R)-treated H9c2 cell model to study the protective effects of coptisine on cardiomyocyte. The results showed that NaS2O4 induced hypoxia/reoxygenation model increased apoptosis and up-regulated autophagy marker LC3-II and cleaved Caspase-3, Beclin1 and Sirt1 levels. Coptisine treatment increased cell survival, inhibited apoptosis, and reduced the protein level of LC3-II, cleaved Caspase-3, Beclin1 and Sirt1. Further, we showed that coptisine combined with chloroquine (CQ), the inhibitor of autolysosome, reduced LC3-II, suggesting that coptisine may inhibit autophagosome formation than induction of autolysosome in the autophagy events. Our results indicate that coptisine may protect cardiomyocyte damage by H/R through suppressing autophagy. Overall, our study provides a new mechanism for the treatment of coptisine on H/R-induced cardiomyocyte damage and death.
Copyright © 2017 Elsevier Inc. All rights reserved.
Apoptosis; Autophagy; Cardiomyocyte; Coptisine; Hypoxia/reoxygenation
Coptisine protects cardiomyocyte against hypoxia/reoxygenation-induced damage via inhibition of autophagy.
Wang Y1, Wang Q2, Zhang L1, Ke Z1, Zhao Y1, Wang D1, Chen H1, Jiang X1, Gu M1, Fan S3, Huang C4.
2017 Aug 19