Relevant bibliographies by topics / Coptisine

Academic literature on the topic 'Coptisine'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Coptisine"

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Zhou, Yan, Chunxiu Zhou, Xutao Zhang, Chi Teng Vong, Yitao Wang, and Wai San Cheang. "Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress." Molecules 26, no. 14 (July 11, 2021): 4210. http://dx.doi.org/10.3390/molecules26144210.

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Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.
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Fu, Shuilian, Saihong Ni, Danni Wang, and Tie Hong. "Coptisine Suppresses Mast Cell Degranulation and Ovalbumin-Induced Allergic Rhinitis." Molecules 23, no. 11 (November 21, 2018): 3039. http://dx.doi.org/10.3390/molecules23113039.

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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.
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Nguyen, Ly Thi Huong, Min-Jin Choi, Heung-Mook Shin, and In-Jun Yang. "Coptisine Alleviates Imiquimod-Induced Psoriasis-like Skin Lesions and Anxiety-like Behavior in Mice." Molecules 27, no. 4 (February 19, 2022): 1412. http://dx.doi.org/10.3390/molecules27041412.

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Psoriasis is a common inflammatory skin disorder, which can be associated with psychological disorders, such as anxiety and depression. This study investigated the efficacy and the mechanism of action of a natural compound coptisine using imiquimod (IMQ)-induced psoriasis mice. Coptisine reduced the severity of psoriasis-like skin lesions, decreased epidermal hyperplasia and the levels of inflammatory cytokines TNF-α, IL-17, and IL-22. Furthermore, coptisine improved IMQ-induced anxiety in mice by increasing the number of entries and time in open arms in the elevated plus maze (EPM) test. Coptisine also lowered the levels of inflammatory cytokines TNF-α and IL-1β in the prefrontal cortex of psoriasis mice. HaCaT keratinocytes and BV2 microglial cells were used to investigate the effects of coptisine in vitro. In M5-treated HaCaT cells, coptisine decreased the production of IL-6, MIP-3α/CCL20, IP-10/CXCL10, and ICAM-1 and suppressed the NF-κB signaling pathway. In LPS-stimulated BV2 cells, coptisine reduced the secretion of TNF-α and IL-1β. These findings suggest that coptisine might be a potential candidate for psoriasis treatment by improving both disease severity and psychological comorbidities.
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Gong, Li-Li, Lian-Hua Fang, Hai-Lin Qin, Yang Lv, and Guan-Hua Du. "Analysis of the Mechanisms Underlying the Vasorelaxant Action of Coptisine in Rat Aortic Rings." American Journal of Chinese Medicine 40, no. 02 (January 2012): 309–20. http://dx.doi.org/10.1142/s0192415x12500243.

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The aim of the present study was to evaluate the vasorelaxant effects of coptisine and its possible mechanisms in isolated rat aortic rings. Coptisine was evaluated on isolated rat aortic rings precontracted with norepinephrine (NE) and KCl. The mechanisms were evaluated in the presence or absence of specific pharmacological inhibitors. Coptisine (1 ~ 200 μM) relaxed NE (1 μM) or KCl (60 mM) induced sustained contraction with pEC50 values of 4.49 ± 0.48 and 4.85 ± 0.57 in a concentration dependent manner. Pretreatment with coptisine (10, 50 or 100 μM) also inhibited concentration-response curves to NE and KCl. The vasorelaxant effect of coptisine was attenuated significantly by endothelium removal, and incubation with Nω-nitro-L-arginine methyl ester (L-NAME, 100 μM), methylene blue (10 μM) and indomethacin (5 μM) partially reduced the vasorelaxant effect of coptisine. In endothelium-denuded rings, the vasorelaxant effect of coptisine was reduced significantly by 4-aminopyridine (4-AP, 100 μM), but not glibenclamide (10 μM) ortetraethylammonium (TEA, 5 mM). Coptisine also reduced NE-induced transient contraction in Ca2+ -free solution, and inhibited contraction induced by increasing external calcium in Ca2+ -free medium plus 60 mM KCl. It was concluded that coptisine induced both endothelium-dependent and -independent relaxation in rat aortic rings. The NO-cGMP mediated pathway may be involved in the endothelium-dependent relaxation and in the activation of voltage-dependent K+ channels, contributing in part to the endothelium-independent relaxation bycoptisine. Coptisine also blocks extracellular Ca2+ influx by interacting with both voltage- and receptor-operated Ca2+ channels.
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Rao, Poorna Chandra, Sajeli Begum, Mahendra Sahai, and D. Saketh Sriram. "Coptisine-induced cell cycle arrest at G2/M phase and reactive oxygen species–dependent mitochondria-mediated apoptosis in non-small-cell lung cancer A549 cells." Tumor Biology 39, no. 3 (March 2017): 101042831769456. http://dx.doi.org/10.1177/1010428317694565.

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This study aimed to explore the effect of coptisine on non-small-cell lung cancer and its mechanism through various in vitro cellular models (A549). Results claimed significant inhibition of proliferation by coptisine against A549, H460, and H2170 cells with IC50 values of 18.09, 29.50, and 21.60 µM, respectively. Also, coptisine exhibited upregulation of pH2AX, cell cycle arrest at G2/M phase, and downregulation of the expression of cyclin B1, cdc2, and cdc25C and upregulation of p21 dose dependently. Furthermore, induction of apoptosis in A549 cells by coptisine was characterized by the activation of caspase 9, caspase 8, and caspase 3, and cleavage of poly adenosine diphosphate ribose polymerase. In addition, coptisine was found to increase reactive oxygen species generation, upregulate Bax/Bcl-2 ratio, disrupt mitochondrial membrane potential, and cause cytochrome c release into the cytosol. Besides, treatment with a reactive oxygen species inhibitor (N-acetyl cysteine) abrogated coptisine-induced growth inhibition, apoptosis, reactive oxygen species generation, and mitochondrial dysfunction. Thus, the mediation of reactive oxygen species in the apoptosis-induced effect of coptisine in A549 cells was corroborated. These findings have offered new insights into the effect and mechanisms of action of coptisine against non-small-cell lung cancer.
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Kim, So Young, Hyun Hwangbo, Hyesook Lee, Cheol Park, Gi-Young Kim, Sung-Kwon Moon, Seok Joong Yun, Wun-Jae Kim, Jaehun Cheong, and Yung Hyun Choi. "Induction of Apoptosis by Coptisine in Hep3B Hepatocellular Carcinoma Cells through Activation of the ROS-Mediated JNK Signaling Pathway." International Journal of Molecular Sciences 21, no. 15 (July 31, 2020): 5502. http://dx.doi.org/10.3390/ijms21155502.

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Hepatocellular carcinoma (HCC) has a high mortality rate worldwide, and treatment is very limited due to its high recurrence and low diagnosis rate, and therefore there is an increasing need to develop more effective drugs to treat HCC. Coptisine is one of the isoquinoline alkaloids, and it has various pharmacological effects. However, the evidence for the molecular mechanism of the anticancer efficacy is still insufficient. Therefore, this study investigated the antiproliferative effect of coptisine on human HCC Hep3B cells and identified the action mechanism. Our results showed that coptisine markedly increased DNA damage and apoptotic cell death, which was associated with induction of death receptor proteins. Coptisine also significantly upregulated expression of proapoptotic Bax protein, downregulated expression of anti-apoptotic Bcl-2 protein, and activated caspase-3, -8, and -9. In addition, coptisine remarkably increased the generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential (MMP), and release of cytochrome c into the cytoplasm. However, N-acetylcysteine (NAC), a ROS scavenger, significantly attenuated the apoptosis-inducing effect of coptisine. It is worth noting that coptisine significantly upregulated phosphorylation of ROS-dependent c-Jun N-terminal kinase (JNK), whereas treatment with JNK inhibitor could suppress an apoptosis-related series event. Taken together, our results suggest that coptisine has an anticancer effect in Hep3B cells through ROS-mediated activation of the JNK signaling pathway.
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Liu, Songcan, Xinfeng Zhang, Furong Qiu, Ping Miao, Shujiao Shen, Leilei Zhu, Jin Zeng, and Jian Jiang. "Metabolic Interaction of the Active Constituents ofCoptis chinensisin Human Liver Microsomes." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/802903.

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Coptis chinensisis commonly used in traditional Chinese medicine. The study investigated metabolic interaction of the active constituents (berberine, coptisine, palmatine, and jatrorrhizine) ofCoptis chinensisin human liver microsomes. After incubation of the four constituents ofCoptis chinensisin HLMs, the metabolism of the four constituents was observed by HPLC. Thein vitroinhibition experiment between the active constituents was conducted, and IC50value was estimated. Coptisine exhibited inhibitions against the formation of the two metabolites of berberine with IC50values of 6.5 and 8.3 μM, respectively. Palmatine and jatrorrhizine showed the weaker inhibitory effect on the formation of the metabolites of berberine. Berberine showed a weak inhibitory effect on the production of coptisine metabolite with an IC50value of 115 μM, and palmatine and jatrorrhizine had little inhibitory effect on the formation of coptisine metabolite. Berberine, coptisine, and jatrorrhizine showed no inhibitory effect on the generation of palmatine metabolite (IC50> 200 μM). The findings suggested that there are different degrees of metabolic interaction between the four components. Coptisine showed the strongest inhibition toward berberine metabolism.
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Zhao, Yaping, and Xia Gao. "Coptisine Reduces the Progression of Cervical Cancer Through Induction of Autophagy." Current Topics in Nutraceutical Research 21, no. 1 (August 10, 2022): 18–24. http://dx.doi.org/10.37290/ctnr2641-452x.21:18-24.

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The regulatory role of coptisine on autophagy in cervical cancer cells (in HcerEpic, HeLa, and SiHa) was examined by assessment of cell viability, colony formation, and apoptosis. Coptisine, in a dose-dependent fashion, significantly inhibited cervical cancer cell viability as measured by cell proliferation, transwell, and TUNEL assays. Coptisine inhibited the levels of p62 and Bcl-2, whilst it promoted the accumulation of Atg5, LC3Ⅱ/LC3Ⅰ and Bax. These data taken together suggest that coptisine inhibits the progression of cervical cancer cells by enhancing autophagy through suppression of the PI3K/AKT/mTOR pathway. This represents a theoretical foundation for developing novel cervical cancer treatments.
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Colombo, Maria Laura, Carlo Bugatti, Andrea Mossa, Nicoletta Pescalli, Laura Piazzoni, Gabriella Pezzoni, Ernesto Menta, et al. "Cytotoxicity evaluation of natural coptisine and synthesis of coptisine from berberine." Il Farmaco 56, no. 5-7 (July 2001): 403–9. http://dx.doi.org/10.1016/s0014-827x(01)01121-1.

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10

Friedemann, Thomas, Udo Schumacher, Yi Tao, Alexander Kai-Man Leung, and Sven Schröder. "Neuroprotective Activity of Coptisine fromCoptis chinensis(Franch)." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/827308.

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Coptis chinensisrhizomes (CR) are one important ingredient of traditional Chinese herbal formulas such as San-Huang-Xie-Xin-Tang which is used for treatment of cardiovascular and neurodegenerative diseases. Recent studies suggest that the extract of CR might be a potential therapeutic agent for amelioration of neurological disorders associated with oxidative stress. In the present study we aimed at revealing the main active compound(s) of the CR extract and at investigating the mechanism of action. Four main alkaloids of the CR extract (berberine, coptisine, jatrorrhizine, and palmatine) were selected for this study. Results showed that out of those alkaloids only pretreatment with coptisine significantly attenuated tert-butylhydroperoxide induced reduction of cell viability, increased rate of apoptosis, and declined mitochondrial membrane potential. Elisa assay and quantitative real-time PCR analyses revealed that thioredoxin-interacting protein (TXNIP) gene expression was downregulated by coptisine, which could explain the neuroprotective effect, hypothetically, by strengthening the thioredoxin defense system against oxidative stress and attenuation of apoptosis signal-regulating kinase (Ask1) mediated apoptotic signaling. A comparison between coptisine and CR extract identified coptisine as the main single component responsible for the neuroprotective effect. Based on the results the CR extract and coptisine are promising candidate agents for prevention or improvement of diabetic neuropathy and neurodegenerative disorders.
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Dissertations / Theses on the topic "Coptisine"

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Papi, Francesco. "Structural investigations on the adducts formed by natural and synthetic compounds with non-canonical DNA foldings." Doctoral thesis, 2018. http://hdl.handle.net/2158/1114320.

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Non-canonical DNA structures are involved in fundamental biological processes as replication, transcription and repair. Their dysregulation is indeed connected to the development of several human diseases, including cancer. As more and more information about their existence and function in living cells are documented, such DNA structures have emerged as promising therapeutic targets. In the last decades, the G-quadruplex folding has caught the attention of scientists because of its implication in the origin and growth of various cancer forms. The stabilization of G-quadruplex structures at human telomeres is thought to be particularly attractive as it might lead to the identification of potential drug candidates with wide-spectrum anticancer activity and reduced side effects in comparison to classical chemotherapies. The research project underlying this thesis concerns the structural investigation on the interaction of non-canonical DNA foldings, especially of the human telomeric G-quadruplex, with natural and synthetic compounds in order to select potential anticancer drugs. The characterization of ligand-DNA adducts has been carried out primarily by X-ray crystallography which provides detailed structural information. In addition, alternative techniques, as CD spectroscopy and in silico calculations, have supplied complementary data with particular reference to the formation of adducts in solution.
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Book chapters on the topic "Coptisine"

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Colombo, M. L., and F. Tomè. "Chelidonium majus L. (Greater Celandine): In Vitro Culture and the Production of Sanguinarine, Coptisine, and Other Isoquinoline Alkaloids." In Medicinal and Aromatic Plants VIII, 157–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-08612-4_8.

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"Coptisine." In Natural Compounds, 418–19. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-0560-3_767.

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